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COLLEGE  OF  PHYSICIANS 
AND  SURGEONS 


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1920 


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FOOD  POISONING 


WORKS  BY 
CHARLES  P.  BOLDUAN,  M.D. 


Immune  Sera. 

Antitoxins,  Agglutinins,  Hemolysins,  Bacterio- 
lysins,  Precipitins,  Cytotoxins,  and  Opsonins, 
Anaphylaxis,  and  Serum  Diagnosis  of  Syphilis. 
Third  edition,  rewritten.  By  Charles  F.  Bolduan, 
M.D.    i2mo,  194  pages.    Cloth,  $1,50, 

Bacterial  Pood  Poisoning. 

A  Concise  Exposition  of  the  Etiology,  Bacteri- 
ology, Pathology,  Symptomatology,  Prophylaxis, 
and  Treatment  of  so-called  Ptomaine  Poisoning. 
By  Professor  Dr.  A.  Dieudonne,  Munich,  Trans- 
lated and  Edited,  with  additions,  by  Dr.  Charles 
F.  Bolduan.    8vo,  127  pages.    Cloth,  $1 ,00. 

The  Suppression  of  Tuberculosis. 

"With  Observations  concerning  Phthisiogenesis 
in  Man  and  Animals,  and  Suggestions  concerning 
the  Hygiene  of  Cow  Stables  and  the  Production 
of  Milk  for  Infant  Feeding,  with  Special  Refer- 
ence to  Tuberculosis.  By  Professor  E.  von 
Behring,  University  of  Marburg.  Authorized 
Translation  by  Charles  F.  Bolduan,  M.D.  i2mo, 
91  pages.    $1,00. 

Manual  of  Serum  Diagnosis. 

By  Doctor  O.  Rostoski,  University  of  Wurzburg. 
Authorized  Translation  by  Charles  F.  Bolduan, 
M.D.    i2mo,  92  pages.    Cloth,  $1,00. 

Collected  Studies  on  Immunity. 

By  Professor  Paul  Ehrlich.  Translated  by 
Charles  F.  Bolduan,  M.D.    8vo,  597  pages.    $6,00, 


E.  B,  TREAT  &  CO.      -      NEW  YORK 


BACTERIAL 

FOOD  POISONING 


A  CONCISE  EXPOSITION  OF  THE  ETIOLOGY,  BACTERI- 
OLOGY, PATHOLOGY,   SYMPTOMATOLOGY, 
PROPHYLAXIS,  AND  TREATMENT  OF 

SO-CALLED    PTOMAINE    POISONING 


PROF.  DR.  A.  DIEUDONNE 

MUNICH 

Translated  and  Edited,  with  Additions,  by 
DR.   CHARLES  FREDERICK  BOLDUAN 
Bacteriologist,   Research  Laboratory,   Department  of  Health, 
City  of  Ne<w  York 

AUTHORIZED     TRANSLATION 


NEW  YORK 

E.  B.  TREAT  &  COMPANY 

1909 


Copyright,  1909, 
By  E.  B.  TREAT  &  COMPANY 


Entered  at  Stationers'  Hall, 
London,  England 


NOTE  BY  THE  AMERICAN  AUTHOR 

Published  less  than  a  year  ago,  Professor  Dieu- 
donne's  manual  on  "  Bacterial  Food  Poisoning "  has 
already  become  favorably  known  as  one  of  the  best 
presentations  of  the  subject.  In  the  present  transla- 
tion, the  editor  has  incorporated  descriptions  of  a 
number  of  additional  outbreaks  of  food  poisoning, 
elaborating  upon  the  prophylaxis  applicable  to  Ameri- 
can conditions,  and  going  more  fully  into  the  details 
of  treatment.  Paragraph  headings  have  also  been 
inserted,  and  the  material  slightly  rearranged,  so  that 
the  same  natural  sequence  is  followed  in  the  different 
chapters.  It  is  believed  that  these  changes,  together 
with  the  index  which  has  been  added,  will  facilitate 
reference  and  still  further  enhance  the  value  of  the 
book. 

Charles  Bolduan. 

New  York,  January,  1909. 


CONTENTS 

PAGE 

INTRODUCTORY      .........  ^ 

I.  MEAT    POISONING.    Poisoning    Through 

Diseased  Meat J5 

Historical 15 

Etiology 20 

Bacteriology 22 

Occurrence  of  the  Bacilli  in  Nature  ...  29 

Biology  of  the  Bacilli 35 

Technique  of  the  Bacteriological  Examina- 
tions     .■ 37 

Clinical  Types  of  Cases.    Symptoms    ...  41 

Diagnosis 44 

Serum  Diagnosis  .» 45 

Prophylaxis 46 

Treatment 47 

II.  MEAT  POISONING  (Continued).    Poison- 

ing Due  to  Eating  of  Decayed  Meat    .     .  48 

Etiology 48 

Symptoms 49 

Bacteria  Found  in  Various  Outbreaks     .     .  50 

Diagnosis 58 

Evidences  of  Putrefaction 59 

Prophylaxis 60 

Treatment 61 

9 


io  CONTENTS 

PAGE 

III.  MEAT    POISONING    (Concluded).      Sau- 

sage Poisoning         62 

Historical 62 

Symptoms 63 

Etiology        66 

Bacteriology 67 

Diagnosis 70 

Prophylaxis 70 

Treatment 71 

IV.  POISONING  THROUGH  FISH  AND  MOL- 

LUSCS       72 

Fish  Poisoning 72 

Clinical  Types  of  Cases.     Symptoms     ...  73 

Mussel  Poisoning 76 

Snail  Poisoning 77 

Poisoning  through  Oysters 78 

Treatment        79 

V.  POISONING  THROUGH  CHEESE    ...  80 

Clinical  Types  of  Cases 80 

Other  Bacteria  Associated  with  Cheese  Poi- 
soning           82 

Treatment 83 

VI.  POISONING    THROUGH     ICE     CREAM 

AND    PUDDINGS      .     . 

Historical    .......    -M 

Bacteriology  .  .,  ,.,  .  m 
Prophylaxis  ..,  L«  .«  ,1  ... 
Treatment   .    -.    w    M    ...    ... 


CONTENTS  ii 

PAGE 

VII.  POTATO  POISONING 91 

Historical 91 

Solanin  Poisoning 92 

Bacteria  Associated  with  Potato  Poisoning  .  95 

Prophylaxis 97 

Treatment 98 

VIII.  POISONING       THROUGH       CANNED 
GOODS 99 

Canning  and  the  Destruction  of  Bacteria    .  99 

Canned  Meats;  Clinical  Types  of  Cases  .     .  99 

Canned  Vegetables 100 

Clinical  Types  of  Cases     .          104 

Bacteriological  Examination 105 

Prophylaxis 106 

Treatment 107 

IX.  METALLIC  POISONS  ........  108 

Historical .  108 

BIBLIOGRAPHY        113 

General    Articles 115 

Meat  Poisoning 116 

Fish  Poisoning 118 

Cheese   Poisoning 119 

Poisoning  through  Ice  Cream  and  Puddings  .  119 

Potato  Poisoning 119 

Poisoning  through  Canned  Goods    ....  120 

INDEX    .......    ;..     .     .     ,.     ,.,    t..    ...  121 


INTRODUCTORY 

Illness  due  to  the  eating  of  infected  foods  is  very 
frequent,  in  fact  far  more  so  than  is  generally  believed, 
for  usually  it  is  only  when  a  large  number  of  such  cases 
occur  that  the  matter  receives  public  notice.  There  is 
little  doubt  that  many  indefinite  infections  and  dis- 
turbances of  the  intestinal  tract,  ordinarily  termed 
errors  in  diet,  are  due  to  the  ingestion  of  decayed  or 
infected  foods. 

At  one  time  most  cases  of  poisoning  through  food- 
stuffs, especially  meat  poisonings,  were  thought  to  be 
true  intoxications  through  putrefactive  substances, 
ptomaines,  etc.  Recent  investigations,  however,  have 
shown  that  they  are  mostly  due  to  certain  specific  bac- 
teria, and  then  either  following  the  introduction  of  the 
specific  pathogenic  bacteria  themselves  (infection),  or 
following  the  introduction  of  the  specific  poisons  pro- 
duced by  the  bacteria  (intoxication). 

It  is  often  a  difficult  matter  to  establish  the  true 
cause  of  a  case  of  food  poisoning,  though,  of  course, 
it  is  easier  when  the  cases  occur  in  large  numbers, 
especially  among  the  inmates  of  barracks,  prisons, 
boarding  schools,  etc.,  where  the  conditions  of  life  are 
uniform  and  readily  controlled.  When  but  one  or  two 
cases  occur  in  a  private  family,  it  is  much  more  diffi- 
cult to  ascertain  the  true  cause,  and  then  only  by  means 


14  INTRODUCTORY 

of  most  painstaking  investigation.  Such  an  investiga- 
tion, moreover,  requires  an  exact  knowledge  of  the 
mode  of  origin  of  these  poisonings,  for  otherwise  the 
subsequent  investigation  will  be  directed  into  entirely 
false  directions.  Besides,  the  bacteriological  examina- 
tion which  is  necessary  in  most  instances,  can  yield  suc- 
cessful results  only  if  the  suspected  material  (remains 
of  the  suspected  food,  stool  or  vomit  of  the  patient, 
etc.)  is  at  once  sent,  properly  packed,  to  the  laboratory. 
The  more  important  of  the  food  poisonings  due  to 
bacteria,  often  occurring  in  extensive  outbreaks,  are  the 
following:  meat  poisoning,  fish  and  shell  fish  poison- 
ing, and  poisoning  through  cheese,  ice  cream,  pud- 
dings, potatoes,  and  canned  goods. 


Bacterial   Food   Poisoning 


MEAT   POISONING 

In  studying  the  poisonings  due  to  the  eating  of  meat 
it  is  well  to  divide  these  into  three  varieties : 

1.  Poisoning  due  to  the  eating  of  meat  from  dis- 
eased animals.  (This  form  is  usually  associated  with 
the  bacillus  enteritidis  or  bacillus  paratyphi.) 

2.  Poisoning  due  to  the  eating  of  putrefied  meat. 
(This  is  usually  associated  with  bacillus  proteus  and 
bacillus  coli.) 

3.  Poisoning  due  to  "  sausage  poison."  (This  is 
produced  by  the  anaerobic  bacillus  botulinus.) 

In  the  first  variety,  poisoning  is  produced  even  by 
freshly-killed  meat ;  in  the  other  two  varieties,  the  meat 
acquires  poisonous  properties  only  after  the  animal 
has  been  slaughtered.  Clinically  the  first  two  varieties 
of  poisoning  manifest  themselves  largely  by  gastro- 
intestinal symptoms,  while  the  third  variety  is  asso- 
ciated especially  with  symptoms  referable  to  the  central 
nervous  system. 

POISONING    THROUGH    DISEASED    MEAT 

Sepsis  Intestinalis    (Bollinger.)     Infectious  Enteritis 

(Gaffky.) 

This  is  the  most  common  of  the  meat  poisonings, 


16  BACTERIAL  FOOD   POISONING 

and  is  due  to  bacteria  of  the  typhoid-colon  group 
(bacillus  enteritidis  and  bacillus  paratyphi  B)  which 
infect  the  animal  during  life.  Although  these  germs 
in  no  way  alter  the  meat,  they  multiply  and  give  rise 
to  poisonous  metabolic  products,  so  that  the  clinical 
symptoms  usually  set  in  after  a  brief  period  of  incu- 
bation. 

HISTORICAL 

One  of  the  first  to  draw  attention  to  this  variety  of 
poisoning  was  Bollinger,  who  described  such  cases  in 
1876.  Five  years  later,  this  author1  was  able  to  report 
on  eleven  large  outbreaks,  embracing  over  1,600  cases. 
The  symptoms  were  chiefly  gastro-intestinal,  but  varied 
considerably  according  to  the  quantity  of  meat  in- 
gested, and  on  the  individual  susceptibility  of  the 
patients.  In  fact,  according  to  Bollinger,  the  symp- 
toms ranged  in  a  complete  scale  from  simple  digestive 
disturbances,  such  as  a  little  gastric  catarrh,  or  per- 
haps a  diarrhoea  with  vomiting,  to  severe  febrile  dis- 
turbances, such  as  those  of  enteritis,  gastric  fever, 
typhoid  fever,  dysentery,  etc.  Dividing  the  cases 
symptomatically,  he  distinguishes  three  groups,  which, 
however,  are  not  sharply  defined  one  from  the  other. 
These  are: — 1,  choleraic  cases  with  profuse  diarrhoeas, 
2,  cases  running  more  of  a  typhoid  course,  with  a 
longer  incubation  than  the  preceding  and  with  marked 
cerebral  disturbances  of  various  kinds,  and,  3,  cases  be- 
ginning with  choleraic  symptoms  but  soon  presenting 
more  the  symptoms  of  typhoid  fever.     If  the  disease 


MEAT    POISONING  17 

is  severe,  convalescence  is  slow,  and  the  patient  is  left 
weak  and  emaciated.  The  duration  of  the  illness  in 
these  cases  is  several  weeks.  In  the  milder  cases,  on 
the  other  hand,  the  disease  only  lasts  a  few  days.  In  the 
fatal  cases  death  usually  occurs  from  the  fourth  or 
fifth  to  the  tenth  or  eleventh  day,  rarely  after  that 
time.  The  autopsy  findings  are  usually  those  of  a 
gastro-enteritis.  The  lymph  nodules  of  the  intestine 
are  very  prone  to  involvement,  ulceration  of  the  intes- 
tine being  of  frequent  occurrence.  The  mesenteric 
glands  may  be  swollen,  and  so  also  the  spleen,  and 
there  may  be  haemorrhages  into  various  organs.  Oc- 
casionally the  entire  anatomical  picture  resembles  that 
found  in  typhoid  fever.  The  period  of  incubation  de- 
pends on  the  amount  of  infected  meat  ingested,  and 
may  vary  from  6  to  24  hours,  to  as  much  as  a  week  or 
more.  Two  epidemic  outbreaks  of  this  form  of  meat 
poisoning  are  described  by  Bollinger  as  being  especially 
interesting,  as  the  symptoms  resembled  those  of  ty- 
phoid fever. 

One  of  the  outbreaks  occurred  in  Andelfingen  in 
1 84 1,  and  embraced  about  450  patients  who  had  come 
together  at  a  musical  festival.  Ten  of  the  patients  died. 
In  all  probability  the  direct  cause  of  the  poisoning  was 
some  roast  veal  which  had  been  eaten  in  large  quantity. 
The  symptoms  were  nausea,  vomiting,  foul-smelling 
diarrhoeas  which  exhausted  the  patients,  dysphagia, 
dilatation  of  the  pupils,  disturbances  of  vision,  delir- 
ium, and  slow  convalescence  with  great  prostration.  It 
was  found  that  persons  who  had  not  attended  the 


18  BACTERIAL  FOOD   POISONING 

festival,  but  who  had  eaten  beef  supplied  by  the  same 
butcher,  also  were  affected,  so  that  it  is  probable  that 
the  infecting  virus  had  been  communicated  from  one 
meat  to  the  other  while  lying  in  the  butcher's  shop. 
Cooking  the  meat  did  not  destroy  the  poison.  The 
period  of  incubation  varied  from  three  to  ten  days. 

The  other  interesting  outbreak  described  by  Bol- 
linger occurred  in  Kloten  in  1878.  Like  the  preceding, 
this  was  associated  with  the  eating  of  meat  at  a  musical 
festival.  Five  hundred  and  ninety-one  of  those  who 
took  part  in  the  festival,  numerous  persons  who  had 
eaten  meat  supplied  by  the  same  butcher,  and  finally, 
also,  a  number  of  persons  in  whom  the  source  of  in- 
fection could  not  be  traced,  a  total  of  657  persons,  were 
thus  poisoned.  Of  these  six  died.  The  direct  cause 
was  found  to  have  been  the  eating  of  the  meat  of  a 
seven-day-old  calf  which  had  been  slaughtered  either 
after  death  or  while  moribund.  In  several  of  the  cases 
the  symptoms  set  in  as  early  as  the  first  day;  in  most, 
however,  there  was  an  incubation  period  of  from  four 
to  six  days.  It  is  interesting  to  note  that  those  who 
drank  wine  freely  either  were  not  affected,  or  suffered 
only  a  mild  attack.  The  symptoms  began  with  de- 
pression, headache,  pains  in  the  limbs,  constipation 
followed  by  diarrhoea.  Toward  the  end  of  the  first 
week  the  cerebral  symptoms  became  less  prominent, 
stools  assumed  more  of  a  typhoid  character,  and  in  the 
severe  cases  there  was  often  a  roseola  and  a  small 
papular  rash.  At  the  height  of  the  disease  there  was 
quite  constantly  an  enlargement  of  the  spleen,  and  the 


MEAT   POISONING  19 

superficial  lymph  nodes,  especially  those  of  the  groin, 
were  frequently  swollen.  A  point  of  considerable  in- 
terest is  the  fact  that  the  outbreak  gave  rise  to  55  sec- 
ondary cases.  The  autopsy  findings  were  enlarged 
spleen,  infiltration  of  Peyer's  patches  and  of  the  soli- 
tary lymph  follicles,  also  ulcers  in  the  small  intestine 
either  in  a  state  of  granulation  or  already  cicatrized. 
On  the  basis  of  the  clinical  symptoms,  as  well  as  of 
the  anatomical  findings,  and  in  view  of  the  fact  that 
secondary  cases  occurred,  most  of  the  observers  re- 
garded the  disease  as  typhoid  fever.  This  opinion  was 
shared  by  Eberth,  who  had  the  opportunity  of  exam- 
ining a  number  of  the  cases  post  mortem.  For  a  con- 
siderable time  there  was  quite  a  difference  of  opinion 
as  to  the  real  nature  of  the  outbreak.  One  set  of  ob- 
servers held  that  it  was  a  true  typhoid  epidemic;  the 
other  regarded  it  as  an  epidemic  of  meat  poisoning. 
Bollinger  believed  that  the  outbreak  was  due  to  a  pe- 
culiar infection  which  closely  resembled  and  in  fact  was 
closely  related  to  typhoid  fever.  He  thought  it  might 
be  regarded  as  a  variety  of  that  disease,  and  proposed 
the  terms  sepsis  intestinalis,  or  septiform  gastroen- 
teritis.    (See  page  15.) 

Numerous  outbreaks  of  meat  poisoning  have  been 
reported  in  the  last  twenty  years.  Ostertag  2  was  able 
to  collect  accounts  of  85  epidemics  in  the  period  1880- 
1900,  the  larger  part  of  which  were  reported  from 
Germany.  The  total  number  of  cases  was  over  4,000. 
There  is  no  doubt,  however,  that  the  actual  number  is 
much  greater,  since  not  all  cases,  even  when  they  occur 


20  BACTERIAL   FOOD   POISONING 

in  considerable  groups,  find  their  way  into  the  litera- 
ture. Bollinger  believes  that  many  cases  of  disease 
giving  the  clinical  picture  of  febrile  jaundice  (Weil's 
Disease)  belong  to  the  group  of  meat  poisonings. 

ETIOLOGY 

Most  of  the  outbreaks  of  this  kind  of  meat  poisoning 
have  been  traced  to  the  meat  of  calves  which  had 
become  septic  from  navel  infection,  or  to  the  meat  of 
cows  which  were  slaughtered  because  they  had  been 
infected  after  calving,  or  were  suffering  from  some 
peculiar  intestinal  or  udder  infection.  Schneidemiihl  4 
has  analyzed  61  large  outbreaks  reported  from  1868  to 
1898,  with  the  following  result.  The  total  number  of 
cases  was  about  5,000,  of  which  76  died.  In  38  of  the 
outbreaks  the  disease  was  traced  to  the  meat  of  cows, 
in  15  to  that  of  calves,  in  3  to  that  of  steers,  in  3  to 
that  of  hogs,  and  in  two  outbreaks  to  horse  meat.  In 
the  case  of  the  cows,  in  16  instances  the  animals  were 
killed  because  of  gastric  and  intestinal  disease;  in  12 
instances,  because  of  disease  of  the  organs  of  parturi- 
tion; in  3  instances  because  of  disease  of  the  udder; 
and  in  3  instances  because  of  foot  and  mouth  disease. 
In  the  case  of  the  calves,  intestinal  and  joint  disease 
were  the  main  reasons  for  slaughtering  the  animals. 
According  to  these  figures,  therefore,  the  chief  source 
of  this  form  of  meat  poisoning  is  the  meat  of  cows 
which  have  been  slaughtered  because  of  disease  of  the 
gastrointestinal  tract,  because  of  septic  infection  after 
calving,  and  septic  infection  of  the  udder.    Next  most 


MEAT    POISONING  21 

dangerous  is  the  meat  of  calves  which  soon  after  birth 
manifest  signs  of  gastrointestinal  disease,  or  pysemic  in- 
fection of  the  joints  (polyarthritis,  phlebitis  of  the 
umbilical  vein).  In  a  case  of  this  form  of  meat  poison- 
ing recently  reported  by  Bryson,55  a  Scotch  shepherd 
became  ill  three  hours  after  eating  some  mutton.  In- 
vestigation showed  that  the  sheep  had  been  ill  for  sev- 
eral days,  and  had  therefore  been  slaughtered.  This 
method  of  disposing  of  sick  animals  is  said  to  be  com- 
mon practice  among  the  Scotch  shepherds,  the  meat 
being  known  as  "  braxy."  The  patient  vomited  re- 
peatedly, had  severe  abdominal  pain,  cramps  in  the 
extremities  and  some  retraction  of  the  head.  There 
was  also  a  slight  rise  of  temperature  the  following  day. 
Within  a  week  the  patient  had  completely  recovered. 

From  the  above  analysis  it  is  apparent  that  the  ma- 
jority of  these  outbreaks  of  epidemic  meat  poisoning 
thus  far  reported  have  been  due  to  what  may  be  called 
"  forced  slaughtering,"  or  "  emergency  slaughtering  " 
of  diseased  animals,  and  allowing  the  meat  to  be  mar- 
keted without  proper  medical  control.  It  has  been 
found  that  usually  the  severest  attacks  followed  the 
eating  of  the  raw  meat,  cooking  destroying  the  in- 
fecting bacteria.  As  a  rule,  however,  cooking  does 
not  destroy  the  toxin  produced  by  these  germs,  though 
there  seem  to  be  some  exceptions  to  this.  Cases  have 
occurred  in  which  the  severest  attacks  were  associated 
with  the  eating  of  the  cooked  meat  and  of  the  resulting 
broth. 

Most  of  the  outbreaks  occur  in  the  summer,  and  in 


22  BACTERIAL   FOOD   POISONING 

many  instances  following  the  eating  of  sausages, 
pates,  chopped  meat,  etc.  These  forms  of  meat  are 
especially  dangerous  because  in  their  manufacture 
viscera,  such  as  lung,  liver  and  spleen,  are  often  em- 
ployed, and  it  is  well  known  that  the  infecting  bacteria 
often  localize  in  these  in  large  numbers.  Furthermore, 
in  consequence  of  the  long  period  which  often  elapses 
from  the  time  of  manufacture  to  that  of  consumption, 
the  bacteria  may  have  abundant  opportunity  to  multiply 
and  produce  their  toxin.  (Van  Ermengem.)  As  a 
rule,  in  contrast  to  what  is  observed  in  "  sausage 
poisoning"  (page  62)  all  of  the  meat  from  these  in- 
fected animals  is  poisonous  immediately  after  slaugh- 
tering; it  may,  to  be  sure,  increase  in  toxicity  as  the~ 
result  of  further  development  of  bacteria  and  conse- 
quent further  toxin  production.  It  is  usually  impossi- 
ble to  distinguish  the  meat  of  such  diseased  animals 
from  that  of  normal  animals  either  by  appearance, 
smell,  taste,  or  consistency.  The  same  is  true  of  the 
dishes  prepared  from  such  infected  meat;  they  appear 
quite  normal.  For  this  reason  the  meat  is  usually  pur- 
chased and  consumed  without  question.  In  the  very 
acute  septic  infections,  the  meat  often  shows  such  slight 
changes  that  unless  one  is  very  familiar  with  the  course 
of  the  disease  and  with  all  its  symptoms,  very  little  is 
found  by  macroscopic  examination. 

BACTERIOLOGY 

Our    knowledge    of    the    etiology    of    the    above- 
described    form    of    meat    poisoning   has    been    aided 


MEAT    POISONING  23 

greatly  by  the  bacteriological  investigations  of  the  past 
twenty  years.  In  all  probability  the  exciting  cause  is 
the  bacillus  discovered  by  Gartner,  the  so-called  B.  en- 
teritidis,  which  is  a  member  of  the  typhoid-colon 
group. 

In  1888  Gartner5  investigated  an  outbreak  of  meat 
poisoning  in  Frankenhausen,  in  which,  two  to  thirty 
hours  after  eating  the  meat  of  an  infected  cow,  57 
persons  became  ill  with  symptoms  of  gastroenteritis. 
One  of  the  persons  died.  The  cow  from  which  the 
meat  was  derived  was  found  to  have  been  slaughtered 
because  of  an  intestinal  catarrh.  Gartner  was  able  to 
isolate  B.  enteritidis  in  pure  culture  not  only  from  the 
infected  meat,  but  also  from  the  spleen  of  the  fatal 
case.  This  organism  is  a  freely-motile  bacillus,  not 
stained  according  to  Gram,  produces  no  indol  in  pep- 
tone solution,  and  ferments  dextrose  with  the  forma- 
tion of  gas.  By  feeding,  and  by  subcutaneous  as  well 
as  intraperitoneal  inoculations  of  pure  cultures,  Gartner 
was  able  to  infect  mice,  guinea-pigs,  rabbits,  sheep  and 
goats.  Cats,  dogs,  and  chickens  proved  refractory. 
The  susceptible  animals  had  fluid  evacuations,  and  on 
post-mortem  examination  showed  a  marked  inflamma- 
tory hyperemia  in  the  intestines  and  abdominal  viscera. 
Frequently  this  was  hemorrhagic  in  character.  The 
lungs  showed  lobular  pneumonic  areas,  and  there  were 
haemorrhages  into  the  organs.  The  bacilli  could  be 
demonstrated  both  microscopically  and  culturally  in 
the  blood  and  internal  organs.  The  B.  enteritidis 
forms  a  poison  which  is  not  destroyed  by  heat ;  guinea- 


24  BACTERIAL  FOOD   POISONING 

pigs  and  rabbits  inoculated  subcutaneously  or  by  mouth 
with  cultures  which  had  been  sterilized  by  heat,  showed 
the  same  symptoms  of  gastroenteritis  as  those  inocu- 
lated with  living  cultures.  In  addition  they  showed 
various  nervous  disturbances,  paralyses  of  the  lower 
extremities  alternating  with  spasmodic  twitchings, 
symptoms  which  are  to  be  regarded  as  signs  of  toxic 
action.  An  interesting  point  in  connection  with  this 
case  is  the  fact  that  the  mother  of  the  dead  boy,  who 
had  nursed  him,  subsequently  developed  the  same  dis- 
ease, although  she  had  not  partaken  either  of  the  meat 
or  the  soup  of  the  infected  cow.  In  other  words,  she 
had  become  infected  from  the  discharges  from  her  son. 

An  interesting  outbreak  is  that  reported  by  G.  Ar- 
buckle  Brown,56  of  Partick,  Scotland,  in  which  twelve 
persons  became  ill  after  eating  canned  meat.  Al- 
though no  bacilli  were  found  in  the  meat,  the  poisoning 
was  probably  due  to  Gartner's  bacillus,  as  the  serum  of 
the  patients  agglutinated  known  cultures  of  this  organ- 
ism in  dilutions  of  1-30  and  1-60.  The  poisoning  in 
this  case  would  appear  to  have  been  caused  only  by  a 
toxin  produced  by  the  bacilli  in  the  meat,  the  organ- 
isms themselves  having  been  killed  during  the  canning 
process,  but  the  toxin  remaining  intact. 

Gaffky  and  Paak  6  in  1885,  i.e.,  three  years  before 
Gartner's  discovery,  had  studied  an  epidemic  of  meat 
poisoning  in  Rohrsdorf,  which  was  traced  to  the  meat 
from  a  horse  suffering  from  abscesses.  Eighty  per- 
sons were  taken  ill,  one  of  whom  died.  The  meat  had 
been  eaten  in  the  form  of  sausage  made  from  the  flesh 


MEAT    POISONING  25 

and  liver  of  the  animal.  The  authors  were  able  to 
cultivate  a  bacillus  from  the  organs  of  animals  inocu- 
lated with  the  sausage.  This  organism  was  subse- 
quently found  to  agree  in  its  important  characteristics 
with  the  bacillus  later  described  by  Gartner,  and  was 
pathogenic  for  animals  in  feeding  experiments.  Un- 
like Gartner's  bacillus,  however,  the  boiled  cultures 
proved  innocuous. 

In  1889  Neelson,  Johne  and  Gartner7  studied  an 
outbreak  of  meat  poisoning  in  Cotta,  near  Dresden, 
which  was  traced  to  a  cow  slaughtered  because  suffer- 
ing from  a  purulent  inflammation  of  the  udder.  There 
were  126  cases,  with  four  deaths.  The  authors  were 
able  to  isolate  a  bacillus  identical  morphologically  and 
culturally  with  the  B.  fenteritidis,  not  only  from  the 
suspected  meat,  and  the  bone  marrow  of  the  cow,  but 
also  from  the  intestinal  tract,  blood,  and  spleen  of  two 
of  the  fatal  cases.  The  bacillus  was  pathogenic  for 
mice  and  guinea-pigs.  The  cultures,  however,  were 
rendered  innocuous  by  boiling,  and  the  same  was  true 
for  the  meat  and  the  soup  made  from  the  same.  In 
passing  it  may  be  said  that  the  toxin  from  B.  en- 
teritidis  does  not  always  withstand  boiling. 

Very  careful  examinations  were  conducted  by  van 
Ermengem  8  in  connection  with  an  epidemic  of  meat 
poisoning  which  occurred  at  Moorseele  in  Flanders,  in 
1 89 1.  Eighty  persons  were  affected,  of  whom  four 
died.  The  outbreak  was  traced  to  the  eating  of 
roasted  and  boiled  meat  derived  from  two  calves  suffer- 
ing from  enteritis.     In  most  instances  the  symptoms 


26  BACTERIAL  FOOD   POISONING 

commenced  within  a  few  hours  after  partaking  of  the 
infected  meat,  although  in  one  of  the  fatal  cases  the 
interval  was  four  days.  Cultures  made  from  the  bone 
marrow  of  the  tibia  of  one  of  the  calves,  and  from  the 
liver,  spleen,  and  intestinal  contents  of  one  of  the  fatal 
cases  revealed  the  presence  of  a  bacillus  which  agreed 
in  all  particulars  with  Gartner's  bacillus.  Cultures 
sterilized  at  ioo°  C.  and  even  at  1200  C.  were  still 
toxic  and  produced  marked  inflammatory  changes  of 
a  hsemorrhagic  character.  Van  Ermengem  called  at- 
tention to  the  similarity  which  B.  enteritidis  bore  to  the 
bacillus  of  swine  plague  and  the  bacillus  of  hog  cholera. 

Hoist 9  studied  an  epidemic  occurring  in  Gaustad, 
near  Christiania,  in  1891.  This  outbreak  was  associ- 
ated with  the  eating  of  meat  from  a  calf  suffering  from 
enteritis.  There  were  81  cases,  with  4  deaths.  Cul- 
tures from  the  spleen  yielded  a  bacillus  which  was 
identical  in  character  with  that  isolated  at  the  Moor- 
seele  outbreak  and  with  known  cultures  of  B.  en- 
teritidis. The  Gaustad  bacillus  produced  toxins  which 
withstood  heating,  but  it  was  found  that  this  property 
was  rapidly  lost  with  artificial  cultivation. 

An  interesting  outbreak  of  meat  poisoning  occurred 
in  Rotterdam  in  1892.  This  was  traced  to  the  meat  of 
a  cow  which  had  been  slaughtered  in  accordance  with 
the  regulations  at  the  municipal  abattoir,  and  which 
had  passed  the  prescribed  inspection  as  normal.  Poels 
and  Dhont 10  were  able  to  isolate  a  bacterium  from  the 
meat,  and  found  that  the  organism  was  pathogenic  for 
mice,  guinea-pigs  and  rabbits,  giving  rise  to  intestinal 


MEAT    POISONING  27 

catarrh,  and  paralysis  of  the  lower  extremities.  Even 
the  sterilized  cultures  were  toxic.  When  small 
amounts  of  the  bacillus  were  injected  intravenously 
into  cows  transient  fever,  muscular  twitchings,  loss  of 
appetite  and  fluid  evacuations  were  produced.  The 
meat  from  these  animals,  slaughtered  four  days  later, 
contained  no  bacilli  and  was  eaten  without  any  in- 
jurious results  whatever.  Another  cow  was  killed  20 
minutes  after  such  an  inoculation.  Small  numbers  of 
the  bacilli  were  found  in  the  spleen,  liver  and  blood. 
After  the  meat  had  been  kept  for  three  days  at  200  C, 
however,  the  number  of  bacilli  present  was  much 
greater.  Some  of  the  meat  had  been  kept  in  the  re- 
frigerator, and  contained  but  few  bacilli.  Fifty-three 
persons  ate  of  this,  and  15  were  attacked  12  to  18  hours 
after  with  headache,  colicky  pains,  and  diarrhoea. 

Basenau  1X  examined  the  meat  of  a  cow  which  had 
been  slaughtered  because  of  illness  after  calving.  He 
isolated  a  bacillus  which  he  termed  B.  bovis  mor- 
bificans,  which  resembled  the  typhoid  bacillus,  was 
pathogenic  in  feeding  experiments,  and  was  killed  by 
exposure  to  70 °  C. 

A  small  epidemic  of  meat  poisoning  occurred  in 
Rumfleth  in  1893.  This  was  traced  to  the  meat  of  a 
cow  which  had  been  ill  for  eight  days  after  calving. 
The  cooked  meat  as  well  as  the  broth  seem  to  have  been 
responsible  for  the  poisoning.  Fischer,12  who  studied 
the  outbreak,  isolated  a  bacillus  from  the  meat  and 
found  it  identical  with  B.  enteritidis.  Injected  into 
animals   it   produced   intestinal   disturbances.     Steril- 


28  BACTERIAL  FOOD   POISONING 

ized  cultures  also  killed  animals  and  produced  similar 
disturbances.  It  was  found,  however,  that  the  toxicity 
rapidly  decreased  with  artificial  cultivation  of  the  or- 
ganism. In  1895,  in  Haustedt,  Fischer  isolated  the 
same  organism  from  the  meat  of  an  ox  which  had  been 
slaughtered  because  suffering  from  diarrhoea.  The 
meat  of  this  animal  produced  symptoms  of  poisoning 
in  50  persons. 

In  1894  an  outbreak  of  meat  poisoning  occurred  in 
Bischofswerde,  Saxony,  almost  100  persons  being 
affected.  The  cause  of  the  poisoning  was  traced  to 
sausages  and  chopped  meat,  composed  of  pork  and 
beef.  There  were  no  deaths.  Johne  13  examined  the 
meat  and  isolated  a  bacillus  closely  related  to  the  B. 
enteritidis. 

In  Ghent,  in  1894,  twelve  persons  became  ill  after 
eating  a  species  of  cervelat  sausage  which  is  eaten  raw. 
The  inspector  having  charge  of  the  abattoir  was  asked 
to  have  an  examination  of  the  sausage  made,  but,  say- 
ing that  there  was  nothing  wrong  with  it,  cut  off  and 
himself  ate  a  few  slices  and  gave  several  to  his  as- 
sistants. The  latter  soon  showed  signs  of  a  more  or 
less  marked  enteritis;  the  inspector  himself  was  at- 
tacked with  severe  choleraic  symptoms,  accompanied 
by  albuminuria,  diarrhoea,  vomiting,  and  collapse,  and 
died  on  the  fifth  day.  Autopsy  showed  a  very  severe 
hemorrhagic  and  gangrenous  gastroenteritis,  fatty 
degeneration  of  the  liver,  acute  interstitial  nephritis, 
etc.  Van  Ermengem 14  examined  the  sausages  bac- 
teriologically,   and   found,   especially   in   the   uneaten 


MEAT    POISONING  29 

part  of  the  sausage  cut  up  by  the  inspector,  a  very 
virulent  and  toxic  bacillus  which  proved  to  be  identical 
with  B.  enteritidis.  The  same  organism  was  isolated 
from  the  blood,  intestine,  and  other  organs  of  the 
inspector.  In  this  outbreak  an  instance  of  direct  trans- 
mission of  the  disease  was  encountered.  The  husband 
of  a  woman  who  had  become  ill  after  eating  some  of 
the  sausage,  himself  became  affected  with  the  same 
symptoms,  although  he  had  not  eaten  any  of  the 
sausage. 

In  recent  years  a  number  of  observers  have  reported 
cases  of  epidemic  meat  poisoning  in  which  bacilli  were 
found  identical  with  B.  enteritidis,  or  at  least  closely 
related  to  that  organism.  The  more  important  of 
these  are  given  in  Table  I.     (See  page  30.) 

In  the  majority  of  these  instances  the  infected  or 
suspected  meat  was  derived  from  diseased  animals  after 
"  forced  slaughtering."  Furthermore,  it  was  repeat- 
edly found  that  the  bacteria  were  present  not  merely 
in  certain  particular  organs,  but  also  in  the  entire 
muscular  tissue,  and  especially  in  the  glandular  organs. 
It  was  not  always  possible  to  demonstrate  the  bacilli 
in  the  suspected  meat,  for  often  there  was  no  material 
left  to  examine.  However,  the  bacilli  were  isolated 
from  the  stools  of  the  patients  and  from  various  organs 
in  the  fatal  cases.  In  the  latter,  they  seemed  to  be 
especially  plentiful  in  the  spleen. 

OCCURRENCE  OF  THE  BACILLI  IN  NATURE 

But  little  is  thus  far  known  concerning  the  occur- 


30 


BACTERIAL  FOOD   POISONING 


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MEAT    POISONING  31 

rence  of  B.  enteritidis  and  B.  paratyphi*  outside  of  the 
infected  organism.  They  do  not  appear  to  be  widely 
distributed.  We  also  know  nothing  as  to  how  these 
bacilli  get  into  the  animal.  Levy  and  Jakobsthal 39 
demonstrated  the  presence  of  true  typhoid  bacilli  in  a 
splenic  abscess  of  a  steer,  so  that  true  typhoid  bacilli 
may  perhaps  also  have  some  relation  to  meat  poisoning. 
In  a  number  of  instances,  the  exciting  organism  was 
found  in  the  organs  of  the  slaughtered  animals 
(Aertryk,  Meirelbeck),  or  in  their  flesh  (Breslau, 
Neunkirchen,  Berlin,  Giessen),  showing  that  the  ani- 
mals had  already  been  infected  during  life.  In  other 
instances,  however,  the  meat  was  originally  sound  and 
was  infected  subsequently.  Sound  meat  is  easily  in- 
fected by  contact  with  meat  containing  these  bacilli, 
especially  if  the  pieces  are  laid  one  on  the  other.  In- 
fection may  also  result  from  infected  persons  handling 
or  preparing  the  meat,  for  now  we  know  that  "  bacilli 
carriers  "  are  not  at  all  uncommon.  In  studying  out- 
breaks of  meat  poisoning  connected  with  restaurants, 
canteens,  and  the  like,  the  existence  of  such  carriers 
must  not  be  forgotten,  and  bacteriological  examina- 
tions of  the  stools  of  such  suspected  carriers  should 
be  undertaken. 

In  order  to  gain  some  idea  as  to  the  occurrence  of 
paratyphoid  and  enteritidis  bacilli,  Dieudonne  recently 
made  some  examinations  among  the  cattle,  calves,  and 
hogs  killed  in  the  Munich  municipal  abattoir.  He  se- 
lected those  which,  for  one  reason  or  another,  had  been 
sent  to  the  sanitary  division  for  further  examination, 
*  For  the   relation  of  paratyphoid  to  enteritidis   see  p.   35. 


32  BACTERIAL  FOOD   POISONING 

especially  animals  with  septic  processes,  such  as  endo- 
metritis, purulent  peritonitis,  suppurative  inflammation 
of  joints  in  calves,  etc.  Recent  investigations  having 
shown  that  typhoid  and  typhoid-like  bacilli  often  are 
especially  numerous  in  the  bile,  cultures  of  this  were 
made  at  once  and  after  enriching  for  24  hours  in  the 
incubator.  The  cultures  were  made  on  malachite- 
green  agar  and  on  Drigalski's  medium.  In  only  a  few 
instances  was  there  any  growth  in  the  cultures  made 
at  once,  and  this  was  due  to  B.  coli,  with  here  and 
there  a  streptococcus.  In  the  cultures  made  after 
enriching  the  bile,  a  profuse  growth  was  always  ob- 
tained. Forty-two  cases  were  examined;  in  thirty-six 
instances  the  growth  was  mainly  streptococcus,  which 
produced  marked  acidity  in  the  medium,  a  few  staphy- 
lococci, and  bacillus  coli.  In  four  instances  bacillus 
coli  alone  was  present,  and  in  two  instances  bacilli  were 
obtained  which  culturally  and  biologically  were  identi- 
cal with  paratyphoid  bacilli.  In  one  of  these  the  cul- 
ture was  obtained  from  a  calf  which  had  become  sep- 
tic from  navel  infection.  Pericarditis  and  joint  inflam- 
mation were  marked.  In  the  other  case  the  animal 
was  a  cow  showing  a  suppurative  peritonitis,  abscesses 
in  the  liver  and  spleen,  and  general  sepsis.  The  bile  of 
both  these  animals  was  mucoid  in  character,  yellow, 
and  quite  thick,  whereas  in  most  of  the  other  animals 
it  was  normal  in  color.  Evidently  we  are  here  dealing 
with  inflammatory  phenomena  with  increased  produc- 
tion of  mucus.  According  to  Pies40  this  favors  the 
growth  of  typhoid  bacilli.     Cultures  made  from  the 


MEAT    POISONING  33 

abscesses  in  the  liver  and  spleen  also  yielded  paraty- 
phoid bacilli,  but  no  bacilli  were  found  in  the  flesh  or 
blood  of  these  animals.  In  abscesses  in  the'  other 
animals  streptococci  were  constantly  present. 

Uhlenhuth  *2  examined  the  intestines  of  apparently 
sound  hogs  killed  in  the  Berlin  abattoir.  In  6%  of 
his  cases  he  isolated  bacilli  which  it  was  impossible  to 
differentiate  either  from  paratyphoid  type  B,  or  from 
bacillus  suipestifer.  These  bacilli,  it  should  be  said, 
are  evidently  very  closely  related,  as  can  be  seen  from 
their  serum  reactions.  Bacillus  paratyphoid  B.  is  also 
a  near  relative  of  the  bacillus  of  mouse  typhoid. 

Similar  investigations  were  undertaken  by  Morgan  57 
in  1905.  This  author  concludes:  "  1.  There  exist 
in  the  intestines  of  healthy  animals  organisms  con- 
forming morphologically  and  biologically  to  the  en- 
teritidis  and  paratyphoid  A  types.  2.  These  organ- 
isms, as  regards  their  agglutination  reactions,  fall  into 
three  groups,  namely,  those  of  the  B.  enteritidis, 
Aertryk,  or  hog  cholera  type,  those  of  the  B.  en- 
teritidis, psittacosis  *  type,  and  those  of  the  B.  para- 
typhoid A,  unknown  type.  3.  The  nomenclature 
adopted  by  different  observers  is  unsatisfactory,  but 
is  based  on  the  principal  differentiating  criterion  we  at 
present  possess,  namely,  specific  virulence." 

Hiibener  61  has  recently  reported  on  the  occurrence 
of  paratyphoid  and  related  bacilli  and  finds  that  not 

*  Psittacosis  is  a  contagious  disease  of  parrots,  communicable 
to  man,  marked  by  pulmonary  disorder  and  high  fever.  The 
organism  is  fully  described  by  Nocard  and  Leclainche,  1898, 


34  BACTERIAL   FOOD   POISONING 

only  do  these  occur  in  the  intestines  of  normal  hogs, 
but  also  occasionally  in  perfectly  sound  sausages,  and 
in  the  excreta  of  healthy  human  beings.  Rimpau 62  ex- 
amined 50  healthy  school  children  and  50  healthy 
orphans  and  found  paratyphoid  bacilli,  type  B.,  in  three 
of  the  former  and  one  of  the  latter.  No  infections 
were  produced  by  any  of  these  bacilli  carriers. 

These  results  are  very  interesting,  for  they  show, 
as  Kutscher  and  Uhlenhuth  emphasize,  that  we  must 
bear  these  diseases  of  animals  in  mind  when  consid- 
ering the  etiology  and  prophylaxis  of  human  paraty- 
phoid infection.  Further  investigations  are  very  much 
desired  concerning  the  relations  existing  between  these 
diseases  and  human  paratyphoid  infections.  Attention 
will  also  have  to  be  paid  to  the  milk  of  such  infected 
animals,  as  has  recently  been  demonstrated  by 
Fischer.41  Investigating  an  epidemic  of  some  50  cases 
exhibiting  the  clinical  picture  of  a  severe  gastro- 
enteritis, this  author  was  able  to  isolate  a  paratyphoid 
bacillus  from  the  stools  of  two  of  the  patients,  and  from 
the  meat,  internal  organs,  and  milk  of  two  cows  which 
had  died  of  gastroenteritis.  Since  none  of  the  meat 
had  been  eaten  by  the  persons  affected,  the  epidemic 
was  ascribed  to  the  drinking  of  the  milk  from  the 
infected  cows. 

Muhlens25a  has  recently  studied  the  occurrence  of 
bacillus  enteritidis,  seeking  especially  to  learn  whether 
this  organism  was  commonly  present  in  food.  Fifty- 
seven  samples  of  different  kinds  of  meat  were  ex- 
amined— pickled   goose   breast,   raw   ham,   pork,   ox 


MEAT    POISONING  35 

tongue,  corned  beef,  smoked  sausage,  smoked  salmon, 
smoked  herring,  etc. — the  samples  were  examined 
culturally,  but  no  bacteria  of  this  group  were  found. 
At  the  same  time  each  of  the  samples  was  fed  to  two 
or  three  white  mice,  the  greatest  care  being  taken  to 
prevent  the  animals  from  infecting  one  another. 
Forty  out  of  the  fifty-seven  samples  killed  one  or  more 
of  the  animals  fed.  From  seventy  out  of  seventy-four 
such  mice  bacteria  belonging  to  the  "  enteritis  "  group 
were  isolated  either  from  the  spleen,  the  blood,  or  the 
intestines.  It  would  seem  that  such  bacteria  may  be 
present  in  very  small  quantity  so  as  to  be  overlooked 
by  cultural  examinations.  Under  favorable  circum- 
stances the  bacteria  may  multiply  in  the  meat  to  a 
sufficient  degree  to  become  pathogenic  for  man,  thus 
causing  the  disease  known  as  "  food  poisoning." 

BIOLOGY  OF  THE  BACILLI 

The  cultural  characteristics  of  the  bacilli  isolated  in 
the  various  outbreaks  are  quite  regularly  similar,  and 
correspond  to  those  of  the  bacillus  enteritidis  and  of 
the  bacillus  first  described  by  Schottmiiller  3I  as  paraty- 
phoid, type  B.  These  bacilli  can  be  distinguished  from 
typhoid  bacilli  and  colon  bacilli  in  a  number  of  ways, 
but  especially  by  their  behavior  to  various  sugars. 
This  is  well  shown  in  Table  II 

From  this  it  will  be  seen  that  B.  enteritidis  and  B. 
paratyphi  B.  ferment  glucose  but  not  lactose;  B.  coli 
ferments  both ;  B.  typhi  ferments  neither. 

An  instructive  table  showing  the  biological  charac- 


36 


BACTERIAL   FOOD   POISONING 


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MEAT    POISONING  37 

teristics  of  the  bacteria  belonging  to  this  group  has  also 
been  prepared  by  Morgan.57 

The  best  medium  for  isolating  these  bacilli  is  the 
malachite-green  agar  of  Lentz  and  Tietz.  On  this  B. 
coli  grows  little  or  not  at  all,  B.  typhi  shows  delicate 
green  colonies  without  discoloring  the  medium,  while 
B.  enteritidis  and  B.  paratyphi  B.  grow  abundantly  and 
change  the  color  to  yellow.  This  medium  might 
therefore  be  called  a  selective  one. 

An  important  means  of  differentiation  is  afforded  by 
the  tests  on  animals,  especially  on  mice  and  guinea- 
pigs.  Typhoid  and  colon  bacilli  are  but  slightly  path- 
ogenic for  these  animals,  whereas  both  enteritidis  and 
paratyphoid  are  markedly  pathogenic.  In  fact,  the 
latter  two  organisms  produce  a  toxin  which  when  given 
per  mouth  kills  susceptible  animals  with  symptoms  of 
gastroenteritis.  This  toxin,  moreover,  is  generally 
quite  resistant  to  the  action  of  heat,  though  here  there 
is  some  individual  variation  in  the  different  cultures. 
This  explains  what  has  already  been  said,  that  infected 
meat,  whether  roasted  or  boiled,  and  even  the  broth 
made  from  such  meat,  may  cause  severe  toxic  symp- 
toms. When  the  bacilli  are  cultivated  for  some  time 
on  artificial  media,  the  virulence  rapidly  decreases,  and 
so  does  the  production  of  the  resistant  toxin. 

TECHNIQUE    OF    THE   BACTERIOLOGICAL   EXAMINATION 

The  isolation  and  identification  of  the  exciting  cause 
of  an  outbreak  of  meat  poisoning  is  quite  a  difficult 
matter,   and  can  be   successfully  performed   only  by 


38  BACTERIAL  FOOD   POISONING 

trained  laboratory  workers.  It  is  extremely  impor- 
tant, therefore,  that  the  required  material  be  properly 
collected,  be  as  fresh  as  possible,  and  then  be  properly 
sent  to  the  laboratory.  The  material  to  be  examined 
will  include  the  suspected  meat  (sausage,  pate,  etc.), 
vomit  and  stool  from  the  patient,  the  patient's  blood, 
and  in  case  of  autopsy,  pieces  of  the  intestine,  spleen, 
and  liver.* 

According  to  Basenau11  it  is  well  to  wait  with  the 
bacteriological  examination  of  the  meat  until  24  hours 
after  slaughtering.  In  that  time  the  bacilli  have  mul- 
tiplied, even  at  the  low  temperature  at  which  the  meat 
is  kept,  so  that  the  bacteriological  examination  is  sim- 
plified. It  is  well  to  select  a  piece  of  meat  rich  in  loose 
areolar  tissue.  The  surface  is  seared  with  a  hot  iron, 
and  then  an  incision  is  made  through  the  seared  area 
with  a  sterile  scalpel.  Smears  and  cultures  are  thus 
made  from  the  inside  of  the  meat.  The  cultures  are 
made  by  smearing  some  of  the  material  with  a  fine 
platinum  loop  over  the  surface  of  gelatine  and  agar 
plates,  over  plates  made  after  the  method  of  Conradi- 
Drigalski,  and  over  malachite-green  plates.  In  pre- 
paring these  plates  it  is  well  to  plate  various  quantities 
of  a  suspension  made  from  the  inside  of  the  suspected 
meat.     Another  portion  of  the  suspected  meat  may  be 

*The  various  materials  should  be  placed  each  in  a  wide- 
mouthed  sterile  bottle  tightly  corked,  the  bottles  packed  with 
ice  and  saw-dust,  and  sent  at  once,  by  special  messenger  if  pos- 
sible, to  the  nearest  laboratory.  All  the  bottles  should  be  care- 
fully labeled  as  to  their  contents,  the  date  of  collection,  and 
a  complete  clinical  account  should  be  sent  to  the  bacteriologist 
for  his  guidance. 


MEAT   POISONING  & 

kept  for  24  hours  at  room  temperature  so  as  to 
"  enrich  "  it,  i.e.,  in  order  to  give  the  bacteria  time  to 
multiply.  After  this,  smears  and  cultures  are  made 
as  with  the  original  specimen.  In  addition  to  this  it 
will  be  well  to  feed  some  of  the  meat  to  mice.  Base- 
nau  "  advises  that  two  mice  be  fed  with  the  meat  raw, 
and  two  mice  with  meat  which  has  been  heated  for  one 
hour  to  ioo°  C.  Mice  are  particularly  well  suited  to 
such  feeding  experiments  because  of  their  extreme  and 
uniform  susceptibility.  The  vomited  material  and  stool 
are  sown  on  plain  agar,  on  Drigalski  medium,  and  on 
malachite-green  plates.  The  last  named  is  very  highly 
spoken  of  for  these  examinations,  as  it  also  in- 
hibits the  growth  of  B.  coli.  Some  of  the  stool  is 
used  for  inoculating  mice  subcutaneously.  The  exam- 
ination of  the  patient's  blood  is  of  considerable  diag- 
nostic significance.  The  most  convenient  method  is  to 
draw  from  5  to  8  cc.  by  means  of  a  sterile  glass  syringe 
and  needle  from  a  vein  at  the  bend  of  the  elbow.  It 
is  unnecessary  to  make  any  incision.  The  skin  is  to  be 
cleansed,  compression  of  the  upper  arm  is  made  by  an 
assistant,  and  the  needle  is  thrust  directly  into  the  dis- 
tended vein.  The  blood  is  distributed  among  a  number 
of  tubes  of  melted  agar,  and  also  planted  into  broth. 
Inoculation  into  bile  medium  has  given  good  results 
in  the  hands  of  several  observers.  A  small  quantity  of 
blood  may  be  left  to  clot  in  the  syringe,  the  serum 
which  separates  being  subsequently  used  to  make  ag- 
glutination tests. 

The  bacteria  isolated  from  the  infected  meat,  from 
the  faeces  of  the  patients,  and  from  the  body  of  the 


4o  BACTERIAL   FOOD   POISONING 

fatal  cases  must  be  tested  by  all  known  methods  of 
differentiation,  including  biological  properties,  patho- 
genicity, and  serum  reactions.  Of  these  the  last  named 
is  the  most  delicate.  The  bacilli  should  be  tested  with 
the  serum  of  an  animal  immunized  against  known  cul- 
ture of  B.  enteritidis  or  B.  paratyphi  B.  In  this  way 
it  is  possible  to  differentiate  these  organisms  from  ty- 
phoid or  colon  bacilli.  Absorption  tests  should  also 
be  undertaken.* 

Extensive  investigations  made  by  de  Nobele,21 
Trautmann,33  Uhlenhuth,  and  others  have  shown  that 
the  bacteria  of  meat  poisoning  may  be  divided  into  two 
types.    According  to  Uhlenhuth  26  these  are  as  follows : 

GROUP  I. 


i 


B.  enteritidis   (Gartner) 

B.  Moorseele    (v.    Ermengem) 

B.  Ghent   (v.  Ermengem)  [    B.  enteritidis,  Gartner, 

B.  Brugge   (v.  Ermengem)  r  group 

B.  Rumfleth  (Fischer) 

B.  Haustedt  (Fischer) 


J 

GROUP  II. 


Paratyphoid  B.  group 


Paratyphoid  B. 
B.  Breslau    (Fliigge-Kansche) 
B.  Meirelbeck  (de  Nobele) 
B.  Diisseldorf   (Trautmann) 
B.  Sirault    (Hermann   &  v.   Ermen- 
gem) 
B.  Aertryk  (de  Nobele) 
B.  Neunkirchen  (v.  Drigalski) 
B.  Greifswald  (Uhlenhuth) 

*The  principle  of  these  is  discussed  in  Bolduan,  "Immune 
Sera,"  Wiley  &  Sons,  N.  Y. 


MEAT    POISONING  41 

Bacilli  of  the  paratyphoid  B.  type  were  also  found  in 
meat  poisonings  in  Alsfeld  (Curschmann),  in  Berlin 
(Kutscher),  in  Bern  (Heller),  and  in  Giessen 
(Fromme). 

CLINICAL   TYPES   OF   CASES 

According  to  van  Ermengem  3  the  clinical  course  of 
the  disease  seen  in  most  of  the  reported  outbreaks 
varied  considerably.  Gastrointestinal  symptoms,  how- 
ever, were  almost  always  prominent.  The  attack  usu- 
ally manifested  itself  like  one  of  cholerine,  or  cholera 
nostras,  or  of  inflammatory  gastroenteritis.  In  addition 
to  the  main  symptoms,  offensive,  yellow,  diarrhceal 
evacuations,  colicky  pains,  vomiting,  and  muscular 
weakness,  there  are  frequently  albuminuria,  catarrhal 
pneumonia,  and  various  cutaneous  lesions,  such  as 
herpes,  polymorphous  erythema,  roseola,  urticaria, 
scurvy-like  haemorrhages  into  the  skin,  or  petechia. 
Dilatation  of  the  pupils,  and  photophobia  have  been  ob- 
served in  some  cases,  and  occasionally  there  has  been 
marked  scaling  of  the  epidermis  on  the  inner  aspect  of 
the  hands  and  soles  of  the  feet.  In  most  instances, 
symptoms  began  in  from  six  to  twelve  hours  after  the 
meat  was  eaten ;  occasionally,  however,  the  interval  was 
much  longer.  In  a  few  cases,  the  vomiting  and  diar- 
rhoea began  immediately  after  the  meal,  just  as  in  an 
ordinary  indigestion.  In  general  it  may  be  said  that 
the  severity  of  the  attack  depends  on  the  amount  of 
meat  eaten.  The  mortality  varies  from  2  to  '5%. 
At  the  autopsy  one  usually  finds  more  or  less  well- 
marked  signs  of  gastroenteritis,  often  hemorrhagic  in 


42  BACTERIAL  FOOD   POISONING 

character.  The  solitary  lymph  follicles  and  Peyer's 
patches  are  swollen  and  prominent;  frequently  there 
are  ulcers  both  in  the  small  and  the  large  intestine. 
The  spleen  is  enlarged,  and  the  kidneys  and  liver  are 
congested.  In  cases  which  have  run  a  rapidly  fatal 
course,  there  are  usually  no  distinct  anatomical 
changes. 

Trautmann,33  struck  by  the  close  biological  relation- 
ship evidently  existing  between  B.  enteritidis  and  the 
paratyphoid  bacillus,  called  attention  to  the  relation  ex- 
isting between  the  respective  diseases  produced  by  these 
organisms,  i.e.,  between  epidemic  meat  poisoning  and 
paratyphoid  fever.  In  meat  poisoning,  as  we  have 
seen,  certain  clinical  as  well  as  pathological  features  are 
distinctly  typhoidal  in  character.  Since  both  diseases 
are  produced  by  the  same  organism,  Trautmann  re- 
gards meat  poisoning  as  a  highly  acute,  and  paraty- 
phoid fever  as  a  more  subacute  form  of  a  common  in- 
fectious disease.  His  explanation  for  the  occurrence 
of  these  two  forms  is  as  follows :  In  meat  poisoning 
the  slaughtered  animal  is  infected,  and  when  the  meat 
is  eaten  both  the  disease  germs  and  their  toxic  products 
poison  the  patient.  The  short  period  of  incubation  in 
meat  poisoning,  as  compared  with  that  in  typhoid  and 
paratyphoid,  is  therefore  due  to  the  large  number  of 
germs  introduced,  and  to  the  fact  that  these  are  ac- 
companied by  their  toxic  products.  If  the  amount  of 
poison  is  too  much  for  the  body  and  if  the  bacteria  in- 
vade the  body  juices,  illness  and  death  follow.  In  para- 
typhoid the  period  of  incubation,  i.e.,  the  time  during 


MEAT    POISONING  43 

which  the  bacilli  multiply  sufficiently  to  produce  toxic 
symptoms,  proceeds  in  the  body  of  the  infected  human. 
The  bacilli  develop  slowly,  and  gradually  give  rise  to 
symptoms  of  illness.  Even  in  meat  poisoning  the  dis- 
ease may  take  a  typhoidal  course.  This  will  occur  when 
but  few  bacteria  and  little  toxin  have  been  ingested.  In 
the  pathological  findings  there  is  considerable  similarity 
between  paratyphoid  fever  and  cases  of  meat  poisoning 
running  a  prolonged  course.  Both  exhibit  the  same 
lack  of  strict  localization  of  the  intestinal  changes,  both 
the  same  hsemorrhagic  character,  and  the  same  main 
symptoms.  Another  point  of  agreement  is  the  remark- 
ably low  mortality  despite  the  severity  of  the  clinical 
symptoms.  According  to  Kayser  34  the  reason  for  the 
short  incubation  period  in  meat  poisoning  as  compared 
to  paratyphoid  is  to  be  found  not  only  in  the  introduc- 
tion of  preformed  toxins,  but  in  the  fact  that  the  path 
of  infection  differs.  Typhoid  and  paratyphoid  fever 
he  regards  as  primarily  a  lymph  and  blood  infection; 
the  intestine  is  affected  secondarily.  In  meat  poison- 
ing, on  the  other  hand,  the  bacilli  reach  the  intestine 
at  once,  and  multiply  there. 

Kutscher,38  moreover,  calls  attention  to  the  fact  that 
in  paratyphoid  infections  not  due  to  meat  poisoning  one 
often  sees  cases  exhibiting  entirely  the  clinical  picture 
of  a  severe  cholera  nostras.  Cases  of  this  kind  have 
been  described  by  Schottmuller,31  and  by  Hetsch.35 
The  latter  observed  a  large  epidemic  of  paratyphoid  in 
Kottbus  in  1905,  and  noted  that  most  of  the  cases  ran 
a  choleraic  course.     Roily  36  divides  the  paratyphoid 


44  BACTERIAL   FOOD   POISONING 

infections  according  to  their  clinical  course,  and  recog- 
nizes two  groups  of  cases,  namely,  cases  presenting  the 
symptoms  of  an  ordinary  typhoid  fever,  and  cases  of 
a  gastric  type,  in  which  gastrointestinal  symptoms  are 
prominent.  He  describes  a  case  of  the  latter  type 
which  ended  fatally,  and  exhibited  the  clinical  picture 
of  cholera  nostras.  This  division  of  the  cases  corre- 
sponds, as  can  be  seen,  with  that  made  by  Bollinger  in 
his  meat  poisonings  in  1881.  Trautmann  states  that 
many  of  the  cases  of  meat  poisoning  seen  in  the  epi- 
demics in  Andelfingen  and  in  Kloten  corresponded 
entirely  to  cases  of  paratyphoid  infection.  The  sim- 
ilarity is  still  more  striking  when  it  is  recalled  that  in 
these  epidemics  instances  of  secondary  infection  oc- 
curred in  persons  who  had  not  eaten  any  of  the  infected 
meat.  These  were  probably  due  to  contact  infection. 
In  the  Kloten  epidemic  the  number  of  secondary  cases 
was  55.  We  see,  therefore,  that  these  more  recent 
etiological  and  bacteriological  investigations  confirm 
the  view  expressed  by  Bollinger  1  in  1881,  namely,  that 
these  forms  of  epidemic  meat  poisoning  are  closely 
related  to  typhoid  fever.  Zupnik 37  speaks  of  those 
varieties  of  meat  poisoning  which  run  a  more  or  less 
marked  typhoid  course  as  "  typhoidal  meat  poisoning." 

DIAGNOSIS 

As  a"  rule  the  diagnosis  of  this  form  of  meat 
poisoning  is  extremely  difficult  unless  a  number  of 
cases  develop  almost  simultaneously.  The  cases  with 
a  long  period  of  incubation  are  especially  liable  to  be 


MEAT    POISONING  45 

overlooked.  In  any  event  the  diagnosis  will  rest  mainly 
on  the  history  of  the  case. 

SERUM   DIAGNOSIS 

The  first  to  employ  serum  diagnosis  in  cases  of  epi- 
demic meat  poisoning  was  Durham,32  who  investigated 
an  outbreak  in  Hatton.  From  the  body  of  a  person 
who  had  died  after  eating  a  meat  pate  Durham  isolated 
a  bacillus  resembling  the  B.  enteritidis,  and  found  that 
it  was  agglutinated  by  the  serum  of  the  other  per- 
sons affected  and  of  the  convalescents  in  dilutions  of 
I :  ioo  to  i :  iooo.  In  subsequent  outbreaks  similar  ob- 
servations were  made.  The  bacillus  isolated  from  the 
suspected  meat  or  from  the  organs  of  the  fatal  cases 
was  agglutinated  by  the  serum  of  the  convalescents  in 
dilutions  of  i  :  500  to  I  :  1000.  The  technique  of  the 
serum  test  is  exactly  the  same  as  that  employed  in  the 
Widal  test  for  typhoid.*  Whenever  possible  the  serum 
of  the  patients  and  of  the  convalescents  should  be 
tested  with  a  reliable  laboratory  culture  of  B.  enter- 
itidis  or  of  B.  paratyphi  B. 

It  is  possible  in  this  way  to  establish  a  diagnosis  of 
epidemic  meat  poisoning  even  after  the  outbreak  has 
passed,  for  the  agglutinating  property  persists  in  the 
blood  of  the  patients  for  several  weeks. 

It  may  be  well  to  say  that  the  bacillus  isolated  is  not 
always  agglutinated  in  as  high  a  dilution  as  a  heterol- 
ogous organism  of  a  closely  related  species.     Thus,  in 

*See  in  Rostoski-Bolduan  "Serum  Diagnosis,"  Wiley  & 
Sons,  New  York. 


46  BACTERIAL  FOOD   POISONING 

a  careful  investigation  of  this  question  in  connection 
with  an  outbreak  due  to  B.  enteritidis,  Liefmann 58 
found  that  the  sera  of  the  patients  agglutinated  typhoid 
bacilli  in  a  higher  dilution  than  the  enteritidis  organ- 
ism isolated  from  the  stools  of  the  patients.  There  was 
conclusive  evidence,  however,  that  the  latter  was  the 
cause  of  the  infection. 

PROPHYLAXIS 

The  prevention,  or  at  least  diminution,  of  this  form 
of  meat  poisoning  can  only  be  effected  by  a  properly 
organized  system  of  meat  inspection,  especially  in  all 
cases  of  "  forced "  or  "  emergency  slaughtering." 
Such  an  inspection  must  embrace  a  careful  and  thor- 
ough examination  of  all  the  organs  by  a  competent 
veterinarian.  It  is  essential  that  all  meat  which  might 
give  rise  to  disease  be  excluded  from  sale  for  human 
consumption.  This  will  include  especially  the  meat  of 
calves  and  cows  which  have  been  slaughtered  because 
of  septic  infection,  and  meat  in  which  abscesses  are 
found  in  the  interior  of  muscles.  Moreover,  since  the 
meat  often  shows  no  macroscopical  changes,  it  will 
be  well  to  adopt  the  suggestions  of  Basenau,  Ostertag, 
v.  Drigalski,  and  others,  and  resort  to  bacteriological 
examinations  in  all  cases  where  there  is  any  suspicion 
that  the  meat  may  be  infected.  Such  examinations 
could  be  made  either  in  a  special  laboratory  connected 
with  the  abattoir,  or  in  one  of  the  regular  hygienic 
laboratories.  In  case  infection  were  demonstrated  by 
this  examination,  the  meat  would  of  course  be  con- 


MEAT    POISONING  47 

demned  and  destroyed.  Ostertag  believes  that  such 
a  laboratory,  would  prove  an  economic  advantage,  for 
if  the  suspected  meat  proved  free  from  infection,  it 
could  be  passed  for  market,  whereas  at  the  present 
time  it  is  customary  to  order  it  condemned,  in  order  to 
be  on  the  safe  side. 

TREATMENT 

The  treatment  of  these  meat  poisonings  will  natu- 
rally depend  on  the  type  of  case  one  is  dealing  with. 
In  the  acute  cases,  with  a  short  period  of  incubation, 
it  is  well  to  wash  out  the  patient's  stomach,  and  this 
plan  should  be  followed  even  though  the  patient  has 
vomited.  During  the  onset  a  brisk  cathartic,  such  as 
castor  oil  or  calomel,  should  be  administered.  Later, 
the  administration  of  stimulants,  especially  alcohol,  is 
indicated.  Alcohol  seems  to  exert  an  inhibitory  action 
on  the  poison,  and  has  given  good  results  in  a  number 
of  reported  cases.  Gastric  irritability  is  treated  with 
sedatives,  mucilaginous  drinks,  cracked  ice,  heat  to  the 
epigastrium,  etc.  The  diarrhoea  is  best  treated  with 
the  initial  dose  of  castor  oil,  followed  by  opium,  rectal 
infusions,  etc.  The  typhoidal  cases  are  treated  exactly 
like  cases  of  typhoid  fever,  and  the  same  precautions 
should  be  observed  to  prevent  infection  of  others. 


II 

MEAT  POISONING— (Continued) 
POISONING  DUE  TO  EATING  DECAYED  MEAT 

ETIOLOGY 

This  variety  of  poisoning  is  due  to  the  eating-  of  meat 
from  healthy  animals,  which  originally  was  sound,  but 
which  subsequently  acquired  toxic  properties,  owing 
to  the  introduction  of  putrefactive  organisms.  This 
form  of  decomposition  may  be  due  to  any  of  the  nu- 
merous putrefactive  bacteria;  as  a  rule,  however,  the 
majority  of  cases  are  due  to  the  members  of  the  proteus 
group  of  organisms  and  to  the  colon  bacillus.  The 
latter  was  isolated  by  Fischer  12  in  cases  of  meat  pois- 
oning, once  from  a  liver  pate,  and  once  from  some  liver 
sausage.  The  colon  bacillus  produces  a  strong  toxin 
which  withstands  heat. 

This  form  of  meat  poisoning  is  observed  chiefly  after 
the  ingestion  of  chopped  meat,  for  this,  almost  in- 
variably, is  rich  in  germs.  Sausages  and  game  are 
also  responsible  for  a  large  number  of  cases.  Putre- 
factive decomposition  of  meat,  however,  does  not  in- 
variably give  rise  to  symptoms  of  poisoning.  This  is 
shown,  for  example,  by  the  extensive  consumption  of 
game  which  is  a  little  "  high."  Which  of  the  putre- 
factive products  is  especially  poisonous,  is  impossible 
to  say.     Further  researches  in  this  direction  are  much 

48 


MEAT    POISONING  49 

desired.  In  all  probability  the  poisoning  is  due  to 
specific  toxins  produced  by  members  of  the  proteus 
group  of  organisms.  These  toxins  are  destroyed  by 
heat. 

Van  Ermengem3  states  that  these  meat  poisonings 
are  much  less  common  after  the  ingestion  of  meat  from 
healthy  animals  which  has  become  infected  after  kill- 
ing than  after  meat  from  diseased  animals  similarly  in- 
fected. Most  of  these  poisonings  are  observed  in  sum- 
mer, probably  because  the  bacteria  can  more  readily 
multiply  in  the  temperature  then  prevailing  outdoors. 
In  many  instances  the  cases  were  due  to  the  eating  of 
chopped  meat.  This  is  often  mixed  with  water  for 
purposes  of  deceit,  and  this  admixture  favors  the 
multiplication  of  the  bacteria. 

SYMPTOMS 

Clinically  this  form  of  poisoning  exhibits  usually  the 
picture  of  an  acute  gastroenteritis  running  a  rapid 
course,  and,  as  a  rule,  without  fever.  The  severity  of 
the  symptoms  depends  on  the  amount  of  meat  eaten, 
and  on  the  age  and  resistance  of  the  patient.  In  most 
instances  the  symptoms  appear  in  from  4  to  20  hours 
after  eating  the  meat,  and  consist  in  vomiting,  head- 
ache, dysenteric,  foul-smelling  stools,  colicky  pains, 
weakness,  etc.  In  more  severe  cases  there  may  be 
convulsions,  pains  in  the  back  and  neck,  and  great  de- 
pression. Most  of  the  cases,  even  the  severe  ones, 
terminate  favorably,  though  a  feeling  of  weakness  may 
persist  for  some  time.     Deaths  are  infrequent. 


SO  BACTERIAL  FOOD  POISONING 

BACTERIA  FOUND  IN  VARIOUS  OUTBREAKS 

According  to  statistics  compiled  by  Schneidemiihl,4 
outbreaks  of  this  form  of  meat  poisoning  were  ob- 
served in  1879  m  Chemnitz,  where  241  persons  became 
ill  after  eating  raw  meat  and  sausage.  Some  of  the 
cases  ended  fatally.  In  1886,  160  persons  became  ill 
in  the  same  city  after  eating  raw  chopped  meat.  The 
meat  was  prepared  during  a  spell  of  very  hot  weather, 
and  had  been  kept  for  some  time.  It  had,  however, 
been  derived  from  healthy  animals.  The  same  meat 
eaten  roasted  or  boiled  was  either  entirely  innocuous 
or  at  the  most  produced  only  transient  malaise.  Haupt 
found  that  this  outbreak  was  due  to  a  variety  of  the 
bacillus  proteus. 

In  1887,  20  persons  became  ill  in  Plauen  after 
having  eaten  raw  chopped  meat  which  had  been 
prepared  six  days  previously  and  was  in  a  state  of  be- 
ginning decomposition.  A  similar  outbreak  is  reported 
from  Gerbstadt  in  which  50  persons  became  ill  after 
eating  raw  chopped  meat,  and  several  kinds  of  bologna 
sausage. 

An  interesting  outbreak  is  described  by  Levy,44  who 
observed  bloody  diarrhoea  and  vomiting  in  18  persons 
frequenting  a  certain  saloon.  It  was  the  custom  here 
to  keep  the  meat  from  day  to  day  in  a  refrigerator 
which  was  found  to  be  covered  with  a  slimy  brown 
crust  having  a  disagreeable  sour  smell.  From  the 
bottom  of  the  ice  box  proteus  bacillus  was  isolated  in 
pure  culture.     The  meat  stored  in  the  box  had  become 


MEAT    POISONING  Si 

infected  with  proteus  and  had  been  the  cause  of  the 
outbreak.  One  of  the  cases  ended  fatally.  At  the 
autopsy  the  bacteria  were  readily  found  in  the  intes- 
tinal contents,  but  not  in  the  blood  of  the  individual. 
When  pure  cultures  of  this  organism  were  injected  into 
animals,  the  clinical  symptoms  produced  resembled 
closely  those  seen  in  the  persons  attacked  during  the 
outbreak.  The  organisms  apparently  did  not  multiply 
in  the  animal  body.  Levy  therefore  believes  that  the 
pathogenic  action  is  not  an  infection,  but  an  intoxica- 
tion, the  proteus  splitting  the  albumins  and  thus  pro- 
ducing a  poison. 

In  1897  Wesenberg45  observed  an  outbreak  of  meat 
poisoning  in  Mansfield,  in  which  63  persons  were  af- 
fected after  eating  chopped  meat.  The  meat  was  de- 
rived from  a  cow  slaughtered  in  an  emergency.  All 
who  had  eaten  the  meat  boiled  or  roasted  remained 
well.  The  persons  affected  had  eaten  the  meat  raw. 
There  were  no  deaths.  Examination  of  the  meat 
showed  the  presence  of  proteus  bacillus  which  was 
highly  virulent  for  test  animals.  It  was  shown  that 
the  meat  became  infected  after  killing;  it  had  been 
stored  in  a  damp  close  cellar,  and  instead  of  hanging 
free  on  hooks,  had  been  piled  together,  piece  on  piece. 

Gliicksmann  46  reports  the  case  of  father  and  son  who 
became  ill  after  eating  from  a  piece  of  half-smoked 
pork.  The  father  died.  Other  persons,  who  had 
eaten  the  same  meat,  but  boiled  or  roasted,  remained 
unaffected.  Examination  of  the  smoked  meat  showed 
the  presence  of  proteus  vulgaris. 


52  BACTERIAL   FOOD   POISONING 

Silberschmidt 4T  described  an  outbreak  of  meat 
poisoning  affecting  44  persons,  one  of  whom  died. 
The  outbreak  was  traced  to  the  eating  of  smoked 
sausages  in  which  large  numbers  of  proteus  bacilli 
were  found.  While  the  smoking  had  not  killed  the 
bacilli,  it  sufficed  to  hide  the  disagreeable  odor  and 
taste  produced  by  these  organisms.  Mice  and  guinea- 
pigs  were  killed  by  feeding  the  infected  sausage; 
proteus  could  not  be  isolated  from  the  organs  of  these 
animals,  but  was  found  in  the  intestinal  contents. 

In  1900  an  outbreak  of  meat  poisoning  occurred 
among  the  troops  in  Hannover.  According  to  A. 
Pfuhl,48  who  observed  this  outbreak,  81  soldiers  were 
attacked  with  symptoms  of  acute  gastroenteritis, 
which,  however,  soon  subsided.  The  poisoning  was 
caused  by  a  peculiar  kind  of  sausage  which,  instead  of 
being  filled  in  sausage  cases,  is  packed  into  jars,  making 
a  kind  of  head  cheese.  In  color,  taste,  and  odor  the 
sausage  appeared  perfectly  normal.  The  bacteriolog- 
ical examination,  however,  disclosed  the  presence  of 
bacillus  proteus. 

In  the  following  year  in  the  same  city  34  persons  be- 
came ill  several  hours  after  eating  this  same  kind  of 
sausage.  The  chief  symptoms  were  nausea,  profuse 
diarrhoea,  repeated  vomiting,  and  considerable  depres- 
sion. In  most  of  the  cases  the  symptoms  subsided 
within  12  hours.  The  sausage  was  examined  by 
Schumburg,49  who  isolated  a  variety  of  proteus.  When 
the  sausage  was  fed  to  mice  and  rats,  the  animals  died 
after    24    hours    with    severe    intestinal    disturbances. 


MEAT    POISONING  53 

Proteus  bacilli  could  also  be  isolated  from  the  organs 
of  these  animals.  Mice  and  rats  fed  with  pure  cultures 
of  the  organism  died  with  symptoms  of  severe  enteritis. 

All  observers  agree  in  believing  that  the  meat  in- 
volved in  these  outbreaks  was  originally  sound,  and 
was  derived  from  sound  animals.  The  proteus  infection 
takes  place  afterwards,  probably  because  the  meat  is 
not  properly  kept.  According  to  the  investigations  of 
Gliicksmann,  Silberschmidt,  and  others,  the  disease  is 
not  merely  an  infection  with  proteus  bacilli,  but  also 
an  intoxication  with  the  metabolic  products  of  these 
organisms.  The  proteus  bacilli  ingested  with  the 
food  multiply  in  the  intestinal  tract  and  produce 
poisons  which  give  rise  to  the  constitutional  symptoms. 
The  intoxication  is  thus  an  accompaniment  of  the  in- 
fection. A  general  infection,  i.e.,  a  flooding  of  the 
body  with  bacteria,  is  probably  very  rare.  This  is 
indicated  by  the  results  of  animal  experiments.  As 
was  stated  above,  animals  infected  with  proteus  die 
with  symptoms  of  severe  enteritis,  yet  the  bacilli  are 
usually  not  found  in  the  organs.  Occasionally  the 
proteus  may  already  have  developed  its  poisonous 
products  in  the  meat.  This,  however,  is  not  often  the 
case,  for  the  odor  of  these  putrefactive  products  would 
at  once  excite  suspicion  (ammonia,  hydrogen  sulphide, 
indol,  etc.).  In  most  of  the  outbreaks  of  meat  poison- 
ing belonging  to  this  group,  we  are  expressly  informed 
that  the  infected  meat  or  sausage  showed  nothing  ab- 
normal in  taste,  odor,  or  appearance. 

While  smoking  does  not  kill  the  proteus  bacillus,  as 


54  BACTERIAL  FOOD  POISONING 

can  be  seen  from  the  case  reported  by  Silberschmidt,  it 
may  occasionally  hide  some  little  disagreeable  odor  or 
taste.  Heating  for  half  an  hour,  to  80 °  C,  on  the 
other  hand,  not  only  kills  the  bacillus,  but  also  destroys 
the  poison  which  it  produces.  In  this  respect  the 
proteus  poison  differs  from  that  produced  by  B.  en- 
teritidis  and  B.  paratyphi. 

An  epidemic  of  meat  poisoning  following  the  eating 
of  potted  tongues  has  recently  been  reported  by 
Berry.62a  The  outbreak  occurred  not  far  from  Liver- 
pool in  the  middle  of  January,  1908,  and  affected  about 
170  persons.  The  symptoms  came  on  36  hours  after 
eating.  In  preparing  "potted  tongue"  the  tongues 
were  first  kept  in  brine  for  three  or  four  days,  then 
cooked,  and  canned  while  hot.  Some  of  the  cooked 
tongue  in  question  was  found  to  be  in  a  bad  state  of 
preservation,  and  smelled  badly.  Bacteriological  ex- 
amination disclosed  the  presence  of  B.  enteritidis  and 
of  an  organism  similar  to  B.  coli.  There  was  some 
evidence  to  show  that  infection  of  the  tongues  had  oc- 
curred in  the  brine. 

It  may  be  mentioned,  in  passing,  that  Ohlmacher 59 
investigated  some  cases  of  poisoning  due  to  eating  oat- 
meal, and  isolated  the  bacillus  proteus  as  the  cause  of 
the  outbreak. 

In  addition  to  the  colon  and  proteus  organisms,  meat 
poisoning  may  occasionally  be  produced  by  the  hay 
bacillus  (B.  subtilis).  An  instance  of  this  is  reported 
by  Lubenau,50  who  observed  an  outbreak  among  the 
inmates  of  the  sanatorium  Beelitz,  in   1906.     About 


MEAT    POISONING  55 

three-quarters  of  the  400  inmates  and  a  large  part  of 
the  help  were  affected  shortly  after  eating  a  dish  known 
as  "  Konigsberger  Klops,"  a  kind  of  meat  croquette. 
This  had  been  served  at  the  noon  meal;  at  about  11 
o'clock  in  the  evening  a  large  number  of  persons  were 
suddenly  seized  with  profuse  diarrhoea,  persistent  vom- 
iting, severe  headache,  and  great  prostration.  In  two 
or  three  individuals  fever  was  also  present.  Most  of 
the  cases  recovered  within  three  or  four  days.  In  a 
few  patients  the  diarrhoea  persisted  for  several  weeks. 
Bacteriological  examination  of  the  meat  balls  revealed 
the  presence  of  a  bacillus  belonging  to  the  hay  bacillus 
group.  Grown  in  milk,  this  organism  produced  a 
strong  poison  which  was  pathogenic  for  young  dogs. 
The  dogs  suffered  from  bloody  diarrhoea  and  vomit- 
ing, and  showed  a  marked  loss  of  weight.  The  or- 
ganism, called  B.  peptonificans,  belongs  to  that  group 
of  hay  bacilli  which  produces  peptone  in  milk,  and 
which  has  been  held  to  be  associated  with  the  intestinal 
disturbances  of  infants.  Investigation  showed  that 
the  meat  balls  had  been  prepared  from  meat  which  had 
been  kept  in  the  refrigerator  for  four  days.  Then, 
since  it  was  still  fresh,  it  had  beeen  parboiled  and  kept 
for  two  more  days  before  using.  The  boiling  had  not 
sufficed  to  kill  the  resistant  spores  of  the  bacilli,  and 
the  temperature  in  the  refrigerator  during  the  last  two 
days  had  been  sufficiently  high  to  allow  the  spores  to 
develop. 

In  view  of  the  extensive  distribution  of  the  proteus 
bacilli,  it  is  curious  that  this  variety  of  meat  poison- 


56  BACTERIAL   FOOD   POISONING 

ing  is  relatively  infrequent.  Very  likely,  however,  it 
is  much  more  frequent  than  the  reports  indicate,  the 
rapid  course  of  the  poisoning  often  causing  the  attack 
to  pass  without  its  nature  being  recognized.  It  is  cer- 
tain that  the  meat  of  animals  slaughtered  in  an  emer- 
gency is  much  more  to  be  feared  than  the  meat  of  sound 
animals.  According  to  Bollinger  four-fifths  of  the 
meat  poisonings  are  due  to  the  former.  The  meat  of 
diseased,  especially  of  septic  animals,  decomposes  very 
readily,  and  is  dangerous  even  when  only  a  slight  de- 
gree of  putrefaction  has  taken  place.  It  is  probable 
that  the  formation  of  poisonous  products  which  has 
begun  during  life,  continues  after  the  meat  has  been 
dressed.  As  a  rule  the  more  rapid  its  putrefaction, 
the  more  poisonous  is  the  meat. 

Owen 60  has  recently  reported  on  an  interesting  out- 
break of  meat  poisoning  which  occurred  in  Kalamazoo, 
Michigan,  in  1906,  and  which  embraced  nineteen  cases. 
Within  a  few  hours  after  eating  the  meat,  the  pa- 
tients complained  of  rapid  pulse,  fever,  and  severe 
abdominal  pains,  with  vomiting  and  purging.  Several 
had  muscular  cramps  in  the  legs ;  one  had  convulsions. 
All  the  patients  made  a  good  recovery  in  a  few  days. 
The  suspected  meat  was  dried  beef,  all  obtained  from 
the  same  butcher,  and  probably  infected  in  his  shop. 
The  meat  had  a  normal  odor  and  appearance,  except 
for  a  slight  greenish  tinge  often  seen  in  sound  meat  of 
this  character.  Emulsions  of  the  meat  were  fatal  when 
injected  into  rats.  Careful  bacteriological  examination 
revealed  a  staphylococcus  as  the  probable  cause  of  the 


MEAT    POISONING  57 

poisoning.  This  organism  was  isolated,  practically  in 
pure  culture,  from  along  the  fasciae,  but  not  in  the  rest 
of  the  meat. 

Although  no  bacteriological  examinations  were 
made,  the  following  recent  outbreak  is  reported  be- 
cause it  suggests  still  another  source  of  bacterial  in- 
fections. In  a  hospital  in  New  York,  fourteen  out  of 
thirty-eight  nurses  suddenly  became  ill  three  or  four 
hours  after  eating  some  minced  chicken.  The  symp- 
toms were  nausea,  vomiting,  prostration,  diarrhoea. 
All  of  the  patients  recovered  by  morning  and  were 
able  to  attend  to  their  regular  duties.  The  chickens 
used  for  preparing  the  minced  chicken  had  been  bought 
as  fresh-killed,  though  it  is  probable  that  some,  at 
least,  were  cold-storage  fowls.  They  were  cooked  on 
Saturday,  and  the  resulting  soup  was  eaten  by  patients 
and  others  without  producing  any  symptoms.  Taken 
out  of  the  soup  caldron,  they  were  kept,  whole,  in  the 
refrigerator  until  Sunday  afternoon,  when  they  were 
cut  up,  minced,  mixed  with  chicken  "  stock "  and 
spices,  and  served  as  minced  chicken  for  the  evening 
meal. 

The  rapidity  with  which  the  symptoms  developed 
point  to  a  preformed  poison  as  the  cause  of  the  out- 
break. It  is  possible  that  chickens  kept  in  cold  stor- 
age for  some  time  become  poisonous  owing  to  the 
bacterial  changes  going  on  even  at  that  temperature.* 

*  The  extent  of  bacterial  growth  which  can  take  place  at 
o°  C.  is  but  little  appreciated.  This  phase  of  the  subject  has 
recently   been    studied   by    Pennington,    who    finds,    for    ex- 


58  BACTERIAL  FOOD   POISONING 

We  know  from  the  investigations  conducted  in  the 
U.  S.  Department  of  Agriculture  by  Pennington  56a  that 
macroscopically  visible  degeneration  does  occur  under 
these  conditions.  Few  bacteriological  investigations 
have  been  made  in  this  direction,*  so  that  at  the  pres- 
ent time  it  is  impossible  to  say  just  what  role,  if  any, 
cold-storage  chickens  play  in  the  causation  of  food 
poisoning.  It  may  not  be  out  of  place  to  call  attention 
to  the  fact  that  the  cold  storage  of  undrawn  chickens, 
game,  etc.,  is  not  at  all  comparable  to  the  keeping  of 
dressed  meats,  such  as  beef,  veal,  pork,  mutton,  etc., 
under  similar  conditions. 

DIAGNOSIS 

The  diagnosis  can  only  be  definitely  established  by 
means  of  bacteriological  examination.  For  this  pur- 
pose plates  should  be  made  from  the  suspected  meat, 
and  animals,  preferably  mice,  infected  by  feeding. 
When  the  poisoning  is  caused  by  bacillus  proteus,  the 
animals  usually  die  in  twenty-four  hours  with  symp- 
toms of  gastroenteritis.  The  germ  can  then  be  isolated 
from  the  intestinal  contents.  It  is  useless  to  examine 
the  meat  chemically  for  the  presence  of  ptomains, 

ample,  that  very  clean  milk  containing  originally  300  germs 
per  cc.  when  kept  for  5  or  6  weeks  at  a  temperature  slightly 
less  than  o°  C,  contains  several  hundred  million  germs  per 
cc.  The  taste  and  odor  of  the  milk  is  not  changed  by  this 
enormous  bacterial  development,  nor  does  the  milk  coagu- 
late on  heating.  (See  Journal  of  Biological  Chemistry,  Vol. 
IV,  1908,  page  353.) 
*  Brown,  H.  R.,  39th  Annual  Report,  Mass-  St.  Bd.  Health. 


MEAT   POISONING  59 

putrefactive  alkaloids,  etc.,  as  such  an  examination 
yields  no  conclusive  information.  The  only  one  compe- 
tent to  properly  deal  with  this  material  is  a  trained 
bacteriologist. 

EVIDENCES  OF  PUTREFACTION 

It  is  sometimes  difficult  to  recognize  beginning 
putrefaction.  The  process  commences  at  the  surface 
and  then  spreads  to  the  deeper  portions.  At  first  the 
connective  tissue  is  affected,  and  extension  is  usually 
along  the  fibrous  tissue,  especially  in  the  neighborhood 
of  a  bone  or  a  large  vessel.  (Schneidemuhl.4)  As 
the  process  continues,  a  thick  greasy-looking  layer  is 
formed  and  a  gradually  increasing  foul  odor  is  given 
off.  When  this  has  continued  for  some  time,  and  con- 
nective tissue  and  muscle  have  completely  disinte- 
grated, putrefaction  is  complete.  The  cut  surface  of 
such  meat  appears  porous,  indentations  made  by  the 
finger  persist,  the  fat,  originally  yellow,  is  greenish, 
the  bone  marrow  is  soft,  or  even  fluid,  and  has  a 
greenish  or  brownish  tint.  The  foul  odor  is  most 
marked  about  the  bones  and  in  the  fat.  This  odor  is 
not  lost  by  boiling  or  roasting  the  meat. 

In  examining  meat  for  evidences  of  putrefaction  it 
is  well  to  first  examine  the  reaction  of  the  meat  to 
litmus,  and  so  seek  to  discover  the  presence  of  some  of 
the  products  of  putrefaction,  such  as  ammonia.  For 
this  purpose  it  suffices  to  lay  a  piece  of  litmus  paper 
on  a  freshly  cut  section  of  the  meat.  This  test  is  not 
always  reliable,  for  corned  beef  and  smoked  ham  give 


6o  BACTERIAL  FOOD   POISONING 

an  alkaline  reaction  even  when  perfectly  sound.  Fur- 
thermore, the  alkaline  reaction  of  putrefaction  may  be 
masked  by  the  acid  products  of  a  fermentation  going 
on  at  the  same  time.  It  is  better,  therefore,  to  test  for 
the  presence  of  free  ammonia  according  to  the  method 
devised  by  Eber.  Into  a  test  tube  about  five  inches  in 
length,  pour  about  half  an  inch  of  a  mixture  composed 
of  one  part  pure  hydrochloric  acid,  three  parts  alcohol, 
and  one  part  ether.  The  mixture  is  shaken  and  then 
a  clean  glass  rod,  rubbed  into  the  suspected  meat,  is 
quickly  thrust  into  the  test  tube,  so  that  the  lower  end 
of  the  rod  is  about  half  an  inch  from  the  surface  of 
the  fluid.  In  the  presence  of  ammonia  one  at  once 
sees  gray,  bluish,  or  whitish  fumes  form  about  the  end 
of  the  rod  and  sink  to  the  surface  of  the  reagent.  This 
test  is  also  not  entirely  free  from  objections,  for  sound 
corned  meat  may  give  a  positive  reaction  owing  to  the 
frequent  presence  of  trimethylamin.  However,  in  the 
presence  of  other  signs  of  putrefaction,  this  test  serves 
to  confirm  the  diagnosis.  In  important  cases  a  bac- 
teriological examination  should  always  be  made. 

PROPHYLAXIS 

In  the  prophylaxis  of  this  form  of  meat  poisoning, 
particular  attention  must  be  paid  to  the  manner  of 
keeping  the  meat.  When  proper  facilities  for  cooling 
are  not  available,  it  is  important  to  eat  the  meat  as 
fresh  as  possible.  Chopped  meat  is  especially  danger- 
ous. Meat  showing  evidences  of  putrefaction  should 
not  be  eaten.    Boiling  and  roasting  or  frying  the  meat 


MEAT    POISONING  61 

lessens  the  danger.  Special  care  should  be  exercised 
in  summer,  when  most  of  these  outbreaks  have  been 
observed.  In  badly  constructed  refrigerators  putrefac- 
tion may  readily  occur.  Owing  to  the  lack  of  venti- 
lation and  the  high  degree  of  moisture,  the  putrefac- 
tive bacteria  may  develop  in  large  numbers.  It  will 
be  recalled  that  in  the  outbreak  reported  by  Levy,  the 
B.  proteus  was  isolated  from  the  bottom  of  the  re- 
frigerator. In  order  to  prevent  putrefaction,  the  re- 
frigerators should  frequently  be  thoroughly  cleansed 
with  hot  soda  solution.  Keeping  meat  in  refrigerators 
poorly  or  not  at  all  iced  is  highly  dangerous.  Edu- 
cation of  the  public  on  this  subject,  and  rigid  inspec- 
tions of  the  meat  markets  by  the  health  authorities 
are  necessary  to  prevent  this  form  of  meat  poisoning. 
Chopped  meat  should  be  especially  well  scrutinized. 
In  view  of  what  has  been  said  above,  it  would  appear 
advisable  to  establish  a  maximum  time  limit  beyond 
which  undrawn  poultry  could  not  be  kept,  even  in  cold 
storage. 

TREATMENT 

The  treatment  of  this  poisoning  is  symptomatic,  and 
consists  in  washing  out  the  stomach,  securing  free 
evacuation  of  the  bowels  by  means  of  cathartics,  and 
administering  stimulants  if  necessary.  Alcohol  ap- 
pears to  be  especially  useful.  In  general  the  treatment 
is  that  outlined  on  page  47. 


Ill 

MEAT   POISONING— (Concluded) 
SAUSAGE  POISONING   (Botulism,  Allantiasis) 

HISTORICAL, 

This  group  of  meat  poisonings,  characterized  by 
severe  nervous  symptoms,  is  usually  spoken  of  as 
"  sausage  poisoning,"  because  most  of  the  cases  re- 
ported followed  the  eating  of  sausages.  Other  forms 
of  food  have,  however,  been  implicated,  and  the  causa- 
tive bacterium,  the  B.  botulinus,  was  isolated  during  an 
outbreak  due  to  poisoning  by  ham.  This  bacillus  is 
a  strict  anaerobe,  and  the  poisonings  are  therefore  ob- 
served in  connection  with  foods  which  have  been  kept 
hermetically  sealed  or  at  least  closed  so  that  air  is 
mostly  excluded.  Furthermore,  it  is  usually  found  that 
the  implicated  articles  have  been  eaten  without  previous 
cooking.  This  includes  particularly  sausages  con- 
tained in  thick  sausage  skins,  to  meat  pates  thickly 
embedded  in  fat,  to  pork  insufficiently  corned,  etc.  In 
most  cases  the  meat  used  in  the  preparation  of  these 
dishes  has  been  found  to  have  come  from  perfectly 
sound  animals.  Other  cases  of  this  form  of  poisoning 
have  been  traced  to  the  eating  of  canned  fish  and 
canned  beans. 

The  first  definite  account  of  sausage  poisoning  was 
published  by  the  poet  and  physician  Justinius  Kerner 

62 


MEAT    POISONING  63 

in  1820,  who  reported  on  a  case  occurring  in  1793 
near  Wildbad,  and  on  a  number  of  epidemics  in  various 
parts  of  Wurttemberg.  The  total  number  of  cases  in- 
volved was  seventy-six,  of  which  thirty-seven  were 
fatal.  (See  Ostertag.2)  In  a  second  publication  in 
1822,  the  author  reports  ninety-eight  additional  cases 
with  thirty-four  deaths.  Since  that  time  a  considerable 
number  of  poisonings  have  occurred  in  Wurttemberg 
after  the  eating  of  liver  sausage,  and  a  sausage  known 
as  "  Schwartemagen,"  although  in  other  countries, 
particularly  in  the  northern  part  of  Germany,  such 
poisonings  are  rare.  According  to  Ostertag  the  reason 
for  this  is  primarily  because  of  the  enormous  extent 
of  the  sausage  industry  and  of  sausage  consumption 
in  Wurttemberg  (especially  as  regards  these  varieties), 
secondly  because  of  the  poor  material  used,  and  finally 
because  of  the  primitive  mode  of  manufacture  in  vogue 
at  that  time.  The  sausages  were  usually  large  in  cali- 
ber, having  been  filled  into  pig  stomach  instead  of  into 
small  gut.  The  smoking  was  therefore  usually  insuf- 
ficient. The  sausages  also  contained  too  much  water. 
Since  the  methods  of  manufacture  have  been  improved 
this  form  of  meat  poisoning  has  been  of  rare  occur- 
rence in  Wurttemberg. 

SYMPTOMS 

The  symptoms  are  very  characteristic,  and  contrast 
sharply  with  those  seen  in  the  other  forms  of  meat 
poisoning.  Whereas,  in  the  latter  the  symptoms  are 
mainly  gastrointestinal,  in  botulism  they  are  almost 


64  BACTERIAL   FOOD   POISONING 

wholly  referable  to  the  central  nervous  system  (v. 
Ermengem),  and  consist  of  secretory  disturbances  and 
symmetrical  motor  paralyses.  The  latter,  either  total 
or  partial,  affect  especially  the  muscles  supplied  by  the 
cranial  nerves,  hence  one  sees  disturbances  of  accom- 
modation, ptosis,  double  vision,  dysphagia,  dryness  in 
the  mouth  and  throat  due  to  inhibition  of  salivary  se- 
cretion, aphonia,  obstinate  constipation,  and  reten- 
tion of  urine.  In  addition  there  are  disturbances  in 
the  heart  action  and  in  respiration.  Fever  is  absent. 
Aside  from  this  there  are  no  motor  or  sensory  paraly- 
ses, and  consciousness  is  unimpaired.  Altogether  the 
symptoms  remind  one  strongly  of  atropine  poisoning. 
As  a  rule  they  appear  in  from  twenty-four  to  thirty- 
six  hours  after  the  infected  meal,  though  sometimes 
the  onset  has  been  within  four  hours,  or  again  not 
until  the  fourth  day.  Death  is  not  uncommon,  and  is 
due  to  asphyxia  of  bulbar  origin.  Many  of  the  other 
cases  take  a  long  course,  of  weeks  or  months.  Even 
when  the  case  terminates  favorably,  disturbances  of 
vision  and  muscular  weakness  persist  for  some  time. 
According  to  some  statistics  collected  by  Senkpiehl, 
out  of  412  cases  which  occurred  from  1789  to  1886, 
there  were  165  deaths,  making  a  mortality  of  about 
40%.  Autopsy  findings  are  almost  entirely  negative; 
usually  all  that  can  be  seen  is  some  hyperemia  of  the 
organs. 

Although  no  bacteriological  examination  was  made, 
the  following  is  probably  an  instance  of  this  form  of 
poisoning.     It  was  reported  by  Sheppard,97  in  1907, 


MEAT    POISONING  65 

and  relates  to  three  fatal  cases.  A  party  of  three  went 
on  a  camping  trip  and  took  with  them  as  part  of  their 
rations  two  cans  of  pork  and  beans.  About  eighteen 
hours  after  eating  of  these  beans,  all  three  became  ill, 
the  symptoms  in  all  being  much  the  same.  "  There 
was,"  says  Sheppard,  "  an  entire  absence  of  the  usual 
gastrointestinal  symptoms  from  first  to  last,  no  pain 
or  sensory  disturbance  and  no  elevation  of  tempera- 
ture. The  first  complaint  was  disturbance  of  vision, 
diplopia  or  a  mistiness  while  looking  in  certain  di- 
rections. Ptosis  was  present  in  two  of  the  cases. 
Thickness  of  speech  and  difficulty  in  swallowing,  which 
later  became  impossible,  were  present  in  all.  Difficult 
breathing  was  also  a  constant  and  common  symptom, 
and  a  general  failure  of  muscular  power;  the  whole 
picture  being  one  of  a  gradually  developing  motor 
paralysis.  A  profuse  secretion  of  mucus  in  the  throat 
was  a  source  of  great  distress,  as  owing  to  the  para- 
lyzed condition  of  the  throat  muscles  it  was  impossible 
to  get  rid  of  it.  The  pulse  until  near  the  end  was  but 
little  altered,  except  for  a  marked  quickening  on  any 
movement  of  the  body.  Temperature  was  normal  or 
subnormal.  Free  purgation  could  not  be  secured,  ow- 
ing presumably  to  the  paralyzed  condition  of  the  in- 
testines in  common  with  the  rest  of  the  body.  The 
kidneys  secreted  freely  an  apparently  normal  urine, 
but  no  examination  of  it  was  made.  The  mental  con- 
dition was  clear  and  undisturbed  to  the  last,  except 
for  an  unnatural  irritability  shown  at  times  when  the 
patients  were  making  an  effort  to  say  something  which 


66  BACTERIAL  FOOD   POISONING 

could  not  be  understood."     Death  occurred  on  the 
fourth  day. 

Investigation  showed  that  the  beans  had  been  pur- 
chased four  months  previously,  and  had  been  kept,  for 
a  time  at  least,  in  rather  a  warm  place.  This  would 
give  infecting  bacteria  opportunity  to  develop  and  pro- 
duce abundant  toxin.  That  such  was  the  case  was 
shown  by  feeding  what  was  left  of  the  beans  to  twelve 
chickens.  Nine  of  these  died,  and  the  other  three  were 
made  ill. 

ETIOLOGY, 

The  cause  of  sausage  poisonings  was  found  by  v.' 
Ermengem  51  to  be  an  anaerobic  bacterium  which  he 
termed  B.  botulinus,  and  which  produces  a  highly  pois- 
onous specific  toxin.  This  organism  was  discovered 
in  a  ham  which  had  caused  fifty  cases  of  "  sausage 
poisoning  "  in  Ellezelles  in  1895,  three  of  the  cases  end- 
ing fatally.  The  bacillus  was  found  in  the  intermuscu- 
lar connective  tissue  in  the  form  of  spores,  but  was  ab- 
sent in  the  fat.  The  same  organism  were  found  in  the 
spleen  and  gastric  contents  of  the  fatal  cases,  though 
here  their  number  was  much  smaller.  The  ham  was 
derived  from  a  hog  which  appeared  perfectly  sound; 
and  that  this  was  the  case  was  indicated  by  the  fact 
that  the  rest  of  the  pork  (eaten  fresh),  as  well  as  the 
other  ham  of  the  same  animal,  were  eaten  without  pro- 
ducing any  toxic  symptoms  whatever.  Further  inves- 
tigation showed  that  the  poisonous  ham  had  been 
corned  and  had  lain  on  the  bottom  of  the  cask  covered 
with  brine ;  the  unaffected  ham  had  been  placed  on  top 


MEAT    POISONING  67 

of  this,  but  had  not  been  covered.  In  the  latter,  there- 
fore, conditions  for  anaerobic  growth  were  not  fav- 
orable. The  poisonous  ham  was  not  putrid,  but  gave 
off  a  marked  rancid  odor  not  unlike  that  of  rancid 
butter.  It  was  also  a  little  discolored,  and  somewhat 
softened.  Watery  extracts  of  the  ham  were  injected 
into  a  number  of  animals  and  produced  typical  symp- 
toms of  botulism.  In  cats  the  symptoms  consisted  of 
marked  mydriasis,  disturbances  of  salivary  secretion, 
various  kinds  of  pareses,  drooping  of  the  tongue, 
aphonia,  dysphagia,  retention  of  urine,  faeces,  and  bile. 
In  pigeons  there  was  paralysis  of  the  wings,  ptosis, 
unequally  dilated  pupils ;  in  monkeys,  guinea-pigs,  rab- 
bits, and  mice  there  were  symptoms  of  general  or  par- 
tial paralysis. 

BACTERIOLOGY 

Bacillus  botulinus  is  quite  a  large  organism,  having 
rounded  ends,  and  producing  oval  spores  situated  in 
the  end  of  the  bacillus.  Motility  is  slight,  and  is  ac- 
complished by  four  to  eight  very  fine  peritrichous 
flagella.  The  bacillus  stains  according  to  Gram,  i.e., 
is  Gram  positive.  It  is  a  strict  anaerobe,  and  grows 
luxuriantly  in  glucose  agar  and  bouillon  with  the  de- 
velopment of  gas.  The  cultures  have  a  rancid  smell 
strongly  resembling  the  odor  of  butyric  acid.  The 
resistance  of  the  spores  is  relatively  slight;  cultures 
containing  spores  are  certainly  killed  by  heating  for 
one  hour  to  80  °  C.  The  bacillus  does  not  develop  in 
media  containing  over  5  to  6%  salt;  hence  it  should 
not  develop  in  properly  corned  meat,  where  the  brine 


68  BACTERIAL  FOOD   POISONING 

contains  10%  salt.  Bacillus  botulinus  produces  a 
strong  toxin.  Filtered  cultures  injected  into  suscep- 
tible animals  such  as  rabbits,  guinea-pigs,  mice,  cats, 
and  monkeys  in  doses  even  as  small  as  o.oooi  cc,  pro- 
duce symptoms  of  paralysis.  Larger  doses  o.i  to  0.5 
cc.  are  rapidly  and  intensely  poisonous.  After  an  in- 
cubation period  of  several  hours,  the  animals  are  often 
seized  with  dyspncea  and  convulsions,  they  fall  on  their 
sides  paralyzed,  and  die  as  a  result  of  rapid  respiratory 
paralysis  in  from  one-quarter  to  half  an  hour.  The 
greater  the  dose  of  toxin,  the  more  rapid  and  severe 
the  development  of  the  symptoms.  There  is,  however, 
a  minimum  beyond  which  the  period  of  incubation  is 
not  affected.  No  matter  how  large  the  dose,  this  is 
never  less  than  from  six  to  twelve  hours.  The  symp- 
toms have  the  character  of  a  pure  intoxication,  with- 
out any  multiplication  of  the  bacilli  in  the  body  taking 
place.  In  contrast  to  what  is  seen  in  most  other 
toxins,  the  toxin  of  this  bacillus  produces  its  symp- 
toms not  merely  after  subcutaneous  or  intravenous 
injections,  but  also  and  especially  after  feeding  per  os. 
In  the  animals  dead  after  such  poisoning,  degenera- 
tion of  the  ganglion  cells  of  the  anterior  horn,  and  of 
the  bulbar  centers  (motor  oculi)  are  observed.  These 
are  the  organs  which  the  clinical  course  of  the  disease 
would  show  were  implicated. 

Kempner 52  immunized  animals  with  botulism  toxin 
and  succeeded  in  preparing  an  antitoxic  serum  which 
possessed  protective  and  also  some  curative  power  in 
animal  experiments. 


MEAT    POISONING  69 

Roemer  53  confirms  all  the  above  observations.  In 
an  investigation  in  1900  he  isolated  B.  botulinus  from 
a  ham  which  had  given  rise  to  typical  symptoms  of 
botulism  poisoning  in  four  persons.  This  ham  came 
from  a  sound  hog,  and  had  been  corned.  So  far  as 
could  be  learned  the  ham  lay  on  top,  but  was  covered 
with  brine.  After  five  weeks  it  was  noticed  that  bub- 
bles of  gas  appeared  in  the  brine.  The  fleshy  part  of 
the  ham  for  the  most  part  was  normal  in  color;  here 
and  there,  however,  there  were  a  few  bluish-gray 
areas,  softer  in  consistency  and  moist.  The  odor  was 
not  putrid,  but  rather  sharply  rancid,  resembling  the 
odor  of  butyric  acid.  No  bacilli  were  found  in  the 
fat  or  in  the  healthy  tissue,  either  by  microscopical  or 
cultural  examination.  From  the  discolored  areas, 
however,  B.  botulinus  was  isolated,  and  also  two  aero- 
bic bacteria.  One  of  these  was  a  large  coccus,  the 
other  a  bacillus  belonging  to  the  hay  bacillus  group. 

Van  Ermengem  also  found  aerobic  bacteria  associated 
with  the  bacillus  botulinus,  and  it  is  likely  that  it  is 
this  association  which  enables  the  latter  organism  to 
develop  anserobically  in  the  brine.  Roemer  found  that 
the  bacillus  does  not  produce  its  poison  in  the  living 
animal  body,  and  that  it  does  not  multiply  either  at 
the  site  of  injection  or  in  the  internal  organs,  or  in 
the  intestine.  In  other  words,  it  is  a  saprophyte,  and 
produces  the  symptoms  entirely  through  the  toxin 
which  it  produced  in  the  infected  meat.  Man  is  poi- 
soned because  the  toxin  is  absorbed  from  the  gastroin- 
testinal tract.     Van  Ermengem  classes  bacillus  botu- 


70  BACTERIAL   FOOD   POISONING 

linus  with  the  "  pathogenic  saprophytes,"  in  order  to 
show  that  although  it  cannot  develop  in  the  living 
animal  body,  it  is  still  pathogenic  through  the  poison 
which  it  produces  in  the  infected  food. 

DIAGNOSIS, 

The  diagnosis  of  botulism  can  only  be  established 
bacteriologically  through  miscroscopical  examinations 
of  the  suspected  meat,  through  anaerobic  cultures  on 
glucose  agar  plates  or  glucose  gelatine,  and  through 
animal  experiments.  The  latter  will  include  feeding 
of  the  meat  to  mice,  feeding  and  inoculating  watery 
extracts  into  rabbits  and  guinea-pigs,  and  testing  the 
toxicity  of  a  several  days'  bouillon  culture  and  of  the 
filtrate  from  such  a  culture  on  these  animals. 

PROPHYLAXIS. 

In  discussing  the  prophylaxis  of  this  variety  of  poi- 
soning, v.  Ermengem  advises  that  such  foods  as  are 
especially  liable  to  botulinus  infection,  such  as  sausages, 
salt  pork,  preserved  meats,  etc.,  should  never  be  eaten 
uncooked.  In  addition  to  this  it  is  important  that  all 
decayed  foods  whose  greasy  appearance,  rancid  or 
butyric  acid-like  odor,  consistency,  or  other  abnormal 
constitution  excites  suspicion,  should  be  destroyed.  In 
corning  meat  the  brine  should  always  contain  sufficient 
salt,  at  least  10%,  for  bacillus  botulinus  cannot  de- 
velop in  brine  of  this  concentration.  In  the  manufac- 
ture of  sausages  and  bologna,  only  sound  meat  and 
organs  should  be  used  which  have  been  thoroughly 
cooked.     The  gut  used  for  sausage  casing  should  be 


MEAT    POISONING  71 

carefully  cleansed,  if  necessary,  with  the  addition  of  a 
harmless  antiseptic.  Schilling  5i  reports  finding  pieces 
of  fecal  masses,  straw,  and  hairs  in  such  sausage  cas- 
ing. In  one  meter  of  gut  he  found  what  was  equal 
to  2  to  16  grams  fluid  faeces.  It  it  well  to  avoid 
sausage  casing  of  very  large  caliber  (beef  or  hog 
stomach),  for  then  it  is  difficult  to  thoroughly  smoke 
the  sausages.  Attention  should  be  paid  to  proper 
smoking.  This  should  be  carried  out  in  suitably  con- 
structed chambers,  and  continuously  until  the  sausages 
are  sufficiently  firm  and  dry.  The  sausages  should  not 
contain  more  than  30  to  35%  water.  In  countries 
where  sausages  are  much  eaten  good  results  have  been 
achieved  by  issuing  proper  instructions  to  the  public 
concerning  the  dangers  from  this  form  of  poisoning, 
and  formulating  suitable  laws  to  carry  into  effect  the 
above  recommendations. 

TREATMENT 

The  treatment  of  botulism  is  essentially  sympto- 
matic, and  consists  in  washing  out  the  patient's 
stomach,  administering  stimulants  subcutaneously,  and 
employing  artificial  respiration  if  necessary.  The 
bowels  may  be  irrigated  with  hot  saline  infusions.  If 
available,  one  may  also  employ  an  antitoxic  serum. 
Such  a  serum  possesses  some  curative  value  in  animal 
experiments,  and  it  can  therefore  be  employed  even 
after  the  onset  of  symptoms.  Wassermann  has  re- 
cently begun  to  supply  such  a  serum  from  the  Institute 
for  Infectious  Diseases  in  Berlin. 


IV 

POISONING  THROUGH  FISH  AND 
MOLLUSCS 

FISH   POISONING 

These  poisonings,  too,  must  be  divided  into  such  in 
which  the  poison  exists  in  the  living  animal  and  such 
in  which  the  poison  develops  subsequently. 

True  poisonous  fish  are  rare  here,  and  are  mostly- 
observed  in  tropical  countries.  Poisoning  occurs  only 
when  the  fish  is  used  for  food.  In  many  species,  e.g., 
in  the  Japanese  fish  "  Fugu,"  the  roe  is  poisonous,  and 
when  eaten  by  man  give  rise  to  choleraic  symptoms, 
paralyses,  and  convulsions  which  are  rapidly  fatal.  It 
is  said  that  if  the  roe  and  all  ovarian  tissue  is  carefully 
removed  from  the  fresh  fish,  no  harm  follows  the 
eating  of  the  fish  itself.  The  poison  is  usually  not 
destroyed  by  boiling.  In  Germany  the  roe  of  barbs 
(Cyprinus  barba)  is  poisonous  when  eaten,  especially 
in  the  month  of  May,  but  the  symptoms  usually  ter- 
minate favorably.  It  is  said  that  the  roe  of  pike,  and 
the  meat  of  sturgeon  {acipenser  huso  and  acipenser 
Ruthenus),  are  also  poisonous  during  the  spawning 
season.  According  to  Robert 63  the  liver,  and  espe- 
cially the  bile,  of  a  number  of  fish  is  poisonous. 

72 


FISH  AND   MOLLUSC   POISONING  73 

CLINICAL  TYPES  OF  CASES 

The  greater  number  of  fish  poisonings,  however,  are 
due  to  bacterial  infection  or  to  intoxication  following 
the  eating  of  diseased  fish  or  of  fish  whose  meat  has 
undergone  post-mortem  putrefaction.  Ulrich64  de- 
scribes an  outbreak  of  fish  poisoning  in  Zurich  in  1904 
that  of  healthy  fish.  Ulrich  found  that  raw  fish,  es- 
the  coast.  The  transportation  of  the  fish  had  taken 
some  days,  and  they  were  kept  from  twenty-four  to 
thirty-six  hours  and  longer  after  cooking.  The  symp- 
toms were  gastroenteric  and  typhoidal  in  character, 
and  varied  in  intensity  according  to  the  interval  elap- 
sing from  the  time  of  catching  the  fish  until  they  were 
eaten.  The  longer  the  interval,  the  severer  the  symp- 
toms. Furthermore,  it  was  noticed  that  some  sound 
fish  kept  on  the  same  platter  as  the  poisonous  ones 
also  become  infected,  and  were  fully  as  dangerous 
as  the  latter.  Wyss  and  Silberschmidt  were  able 
to  isolate  the  paratyphoid  bacillus  B.  from  the  blood 
of  two  of  the  persons  who  died.  The  blood  of 
the  other  patients  agglutinated  this  bacillus.  It  was 
impossible  to  determine  whether  the  living  fish  had 
been  infected  with  the  organism.  It  may  be  assumed, 
however,  that  the  flesh  of  diseased  fish  is  more  suitable 
for  the  development  of  pathogenic  bacteria  than  is 
which  was  probably  caused  by  some  pike  shipped  from 
pecially  in  summer,  contains  a  large  number  of  bac- 
teria, particularly  members  of  the  colon  and  proteus 
groups.     Ordinary  boiling  does  not  suffice  to  kill  all 


74  BACTERIAL  FOOD   POISONING 

the  bacteria,  and  if  the  fish  is  kept  for  some  time  after 
cooking,  especially  in  summer,  bacterial  multiplication 
is  rapid.  When  large  numbers  of  bacteria  are  thus 
taken  with  the  food,  severe  gastric  disturbances  may 
be  produced.  In  this  respect  colon  infection  is  much 
more  dangerous  than  proteus,  for  with  the  latter,  pu- 
trefactive changes  (putrid  odor)  soon  manifest  them- 
selves, which  is  not  the  case  in  colon  infections.  The 
paratyphoid  bacillus  isolated  from  the  fish  grows  luxu- 
riantly in  fish  meat.  Owing  to  the  rapid  multiplication 
of  bacteria  in  cooked  fish  at  warm  temperatures,  Ulrich 
regards  the  eating  of  fish  in  summer  as  dangerous 
when  more  than  twenty-four  hours  have  elapsed  since 
the  cooking. 

In  1906  an  outbreak  of  fish  poisoning  was  reported 
by  Abraham.65  This  embraced  twenty-eight  cases 
which  developed  eighteen  hours  after  eating  some 
pike.  The  symptoms  were  fever,  intestinal  colic, 
mild  diarrhoea,  and  nausea.  After  two  to  three  days 
the  fever  subsided,  the  colic  and  diarrhoea  ceased,  and 
the  patients  were  entirely  well  at  the  end  of  a  week. 
The  piece  of  fish  that  was  left  over  showed  nothing 
abnormal  either  in  color,  odor,  or  taste.  The  bac- 
teriological examination  made  by  Neisser  disclosed  the 
presence  of  a  bacillus  belonging  to  the  paratyphoid 
group,  type  Aertryk.  This  organism  produces  a  toxin 
which  withstands  considerable  heating.  Serum  exam- 
inations conducted  on  the  blood  of  a  number  of  the  pa- 
tients gave  positive  results  with  this  bacillus.  No 
such  bacilli  could  be  found  in  the  stools  of  the  pa- 


FISH   AND   MOLLUSC   POISONING  75 

tients.  In  this  case  it  was  believed  that  the  fish  had 
become  infected  during  life,  the  bacilli  lodging  in  the 
flesh,  and  thus  causing  the  infection  in  the  persons  who 
ate  of  the  meat.  In  view  of  the  fact  that  the  pike  is  a 
voracious  feeder,  spends  considerable  time  about  the 
mouth  of  sewers,  and  also  feeds  on  other  cadavers,  it 
is  quite  conceivable  that  pathogenic  bacteria  such  as 
the  paratyphoid  bacilli  may  gain  entrance  into  his 
body. 

In  addition  to  these  two  forms  of  poisoning,  one 
meets  with  cases  of  fish  poisoning  whose  course  is  much 
like  that  described  under  botulism.  Such  cases  usu- 
ally follow  the  eating  of  canned  fish  or  lobster  when 
the  can  has  remained  standing  open  for  some  time. 
In  some  instances  it  is  probable  that  the  poison  was 
contained  in  the  mayonnaise  dressing.  It  is  not  un- 
likely that  the  numerous  attacks  of  indigestion  follow- 
ing the  eating  of  lobster  salad  are  in  part  due  to  such 
poisons. 

Severe  illness  has  often  followed  the  eating  of  crabs. 
It  has  been  found  that  poisonous  substances  sometimes 
develop  in  boiled  crabs,  on  standing,  even  before  the 
appearance  of  a  putrid  odor.  This  is  especially  true 
when  the  animals  have  been  boiled  after  death 
(Schneidemuhl 4).  The  symptoms  which  have  been 
observed  with  this  form  of  poisoning  were  lassitude, 
dragging  pains  in  the  back,  and  painful  stiffness  in 
the  limbs. 

Convalescence  was  protracted,  sometimes  lasting 
months. 


76  BACTERIAL  FOOD   POISONING 

MUSSEL  POISONING 

In  1885  an  outbreak  of  poisoning  occurred  in  Wil- 
helmshaven  following  the  eating  of  common  mussels 
(Mytilus  edulis) .  There  was  no  evidence  of  putrefac- 
tion. In  most  of  the  cases,  the  symptoms  appeared  in 
from  one-quarter  to  one-half  an  hour  after  the  meal, 
and  consisted  in  a  feeling  of  constriction  in  the  throat, 
itching  of  the  extremities,  dizziness,  marked  weakness. 
In  the  fatal  cases  death  occurred  in  from  two  to  five 
hours.  At  the  autopsy  Virchow  constantly  found  an 
enlarged  spleen,  and  fatty  degeneration  of  the  kidney 
and  liver.  Fatal  cases  of  this  form  of  poisoning  have 
been  reported  by  other  observers.  Brieger  succeeded 
in  isolating  a  poisonous  alkaloid  which  he  termed 
mytilotoxin,  and  whose  action  was  very  similar  to 
that  of  curare.  He  found  that  the  poison  could  be 
destroyed  by  boiling  with  water  containing  three  to 
five  grams  of  sodium  carbonate  per  liter.  It  is  not 
known  how  this  poison  originates.  In  most  instances 
it  is  said  that  the  poisonous  mussels  came  from  stag- 
nant water.  Schmidtmann  found  that  sound,  non- 
poisonous  mussels  placed  in  the  water  of  the  canal  from 
which  the  poisonous  mussels  had  been  derived,  acquired 
toxic  properties;  and  conversely,  when  the  poisonous 
mussels  were  kept  in  the  clean  water  of  the  bay,  they 
rapidly  lost  all  trace  of  poison.  He  therefore  as- 
sumed that  bacteria  present  in  the  canal  water  gave 
rise  to  the  poison  in  the  mussels.  Schmidtmann  states 
that  poisonous  mussels  possess  a  sweetish,  nauseating, 


FISH  AND   MOLLUSC  POISONING  77 

bouillon  odor,  while  sound  mussels  have  the  odor  of 
fresh  sea  water.  Lustig  and  Zardo  isolated  two  dif- 
ferent varieties  of  bacteria  from  mussels,  and  found 
the  cultures  virulent  for  animals.  They  did  not  es- 
tablish the  identity  of  these  organisms. 

SNAIL    POISONING. 

A  kind  of  marine  snail,  Murex  bradatus,  has  also 
been  the  cause  of  poisonings  of  this  kind.  Such  an 
outbreak  was  reported  in  1900,  in  Isola,  by  Galeotti 
and  Zardo.66  Forty-three  persons  were  affected,  the 
symptoms  being  severe  vomiting,  hematuria,  convul- 
sions, paralyses,  and  diarrhoea.  In  some  of  the  severest 
cases  constipation  was  observed.  Five  of  the  persons 
died,  and  the  autopsy  revealed  the  presence  of  nu- 
erous  haemorrhages  scattered  through  the  subcutane- 
ous connective  tissue,  the  muscles,  serous  membranes, 
and  heart.  There  was  also  fatty  degeneration  of  the 
liver,  heart,  and  kidneys.  From  a  number  of  the  other 
snails  captured  in  the  same  locality  the  observers  iso- 
lated a  bacillus  related  to  the  bacillus  of  hemorrhagic 
septicaemia.  This  organism  was  highly  virulent  and 
was  toxic  even  in  feeding  experiments.  Animals 
killed  in  this  way  exhibited  pathological  changes  very 
like  those  found  in  the  human  autopsies.  Investiga- 
tion showed  that  this  bacillus  was  probably  a  common 
normal  inhabitant  of  the  molluscs  in  those  waters, 
and  that  it  in  some  way  acquired  pathogenic  properties 
for  humans. 

It  must  not  be  forgotten,  however,  that  many  of 


78  BACTERIAL  FOOD   POISONING 

these  mussel  and  sea  snail  intoxications  are  due  to 
changes  caused  by  proteus  and  other  putrefactive  bac- 
teria. 

POISONING   THROUGH    OYSTERS 

Oysters  have  also  frequently  been  the  cause  of  in- 
toxications, especially  when  the  oyster  beds  are  located 
near  the  mouths  of  sewers,  or  when  the  oysters  are 
fattened  in  such  waters.  According  to  Bardet,  prac- 
tically all  oysters  are  diseased  during  the  summer 
months.  Furthermore,  oysters  very  readily  spoil,  and 
the  eating  of  such  oysters  is  very  dangerous.  The 
symptoms  produced  vary  considerably.  Sometimes  the 
poisoning  takes  the  form  of  an  urticaria,  sometimes 
that  of  a  severe  gastroenteritis,  and  fatal  cases  running 
a  course  like  that  of  botulism  have  been  described.  The 
bacteriological  investigations  which  have  been  made 
in  these  cases  have  not  yielded  definite  results.  Ty- 
phoid fever  and  cholera  may  also  be  spread  by  the  eat- 
ing of  infected  oysters,  especially  when  the  waters 
from  which  the  oysters  come  are  polluted  by  sewage. 
A  number  of  outbreaks  of  typhoid  fever,  or  a  disease 
resembling  this,  have  been  traced  to  the  eating  of 
oysters,  but  in  only  very  few  instances  was  the  typhoid 
bacillus  really  demonstrated.  On  the  other  hand, 
bacillus  coli  has  repeatedly  been  found  in  oysters,  and 
this  has  been  taken  as  indicating  fecal  pollution.  Other 
authors  have  interpreted  this  quite  differently,  saying 
that  colon  bacilli  are  a  common  normal  inhabitant  of 
these  shell  fish.  Bacilli  belonging  to  the  proteus  group 
have  also  been  demonstrated  in  oysters,  and  Vivaldi 


FISH  AND   MOLLUSC   POISONING  79 

and  Rodella 67  isolated  a  bacillus  resembling  B.  coli, 
and  belonging  to  the  group  of  capsule  bacilli.  This 
was  pathogenic  for  humans.  It  is  absolutely  necessary 
that  oyster  beds  be  located  only  where  fecal  contami- 
nation from  sewers,  etc.,  can  be  excluded.  Furthermore, 
it  is  important  that  oysters,  clams,  and  other  shell  fish 
be  eaten  only  when  fresh.  Travelers  should  be  par- 
ticularly careful,  especially  in  southern  countries,  for 
many  a  person  has  become  infected  with  typhoid  fever 
or  suffered  from  some  grave  intestinal  disorder  by  the 
indiscriminate  eating  of  shell  fish  while  traveling. 
One  should  always  hesitate  when  the  oysters  are  of- 
fered at  especially  low  prices,  for  this  is  often  merely 
a  means  of  disposing  of  stale  or  otherwise  undesirable 
wares.  Attention  should  be  paid  to  signs  indicating 
dead  oysters  (gaping  shell),  and  to  indications  of 
putrefaction  (discoloration  and  softening,  with  a  black 
ring  on  the  inner  side  of  the  shell.  Vagedes68). 
Poisoning  through  oysters  is  especially  frequent  dur- 
ing the  summer  months,  whence  comes  the  custom  of 
eating  them  only  during  months  whose  names  con- 
tain an  R. 

TREATMENT 

The  treatment  of  these  poisonings  does  not  differ 
in  general  from  that  outlined  under  meat  poisoning 
on  page  47,  and  under  botulism  on  page  71.  Cases 
running  a  typhoidal  course  should  be  treated  exactly 
like  typhoid  fever,  and  the  same  precautions  should  be 
observed. 


V 

POISONING  THROUGH  CHEESE 

CLINICAL  TYPES  OF  CASES 

Poisoning  due  to  the  eating  of  infected  cheese  has 
been  reported  repeatedly.  The  ordinary  symptoms  are 
diarrhoea  and  vomiting,  and  in  severe  cases  vomiting 
of  blood,  rectal  tenesmus,  collapse.  In  some  instances 
there  were  disturbances  of  vision,  or  taste,  dryness  in 
the  throat,  obstinate  constipation,  etc.,  symptoms,  in 
other  words,  much  like  those  of  botulism.  As  a  rule 
nothing  peculiar  was  noted  about  the  taste  of  the 
cheese,  except  that  it  was  sometimes  somewhat  bitter. 
The  cause  of  this  form  of  poisoning  was  formerly 
believed  to  be  a  poisonous  alkaloid  discovered  by 
Vaughan,  and  termed  by  him  tyrotoxicon.  But  re- 
cent investigations  have  repeatedly  shown  bacteria  to 
be  the  cause  of  such  poisonings.  In  an  outbreak  de- 
scribed by  Vaughan  and  Perkins,69  twelve  persons 
became  ill  three  to  six  hours  after  eating,  with  nausea, 
vomiting,  pains  in  the  abdomen,  and  threatened  heart 
failure.  Some  of  the  patients  had  dilated  pupils  and 
some  even  were  delirious.  The  authors  were  able 
to  isolate  a  bacillus  from  the  suspected  samples,  and 
found  this  to  be  pathogenic  for  the  ordinary  laboratory 

animals.     The  bacillus  produced  a  strong  toxin.     By 

80 


POISONING  THROUGH   CHEESE  81 

mistake  a  patient  was  injected  with  ten  drops  of  a  steril- 
ized culture  of  the  bacillus  in  milk.  Within  thirty- 
minutes  the  patient  complained  of  dizziness,  vomited 
freely,  and  had  severe  diarrhoea.  Two  hours  after  the 
injection  he  was  almost  entirely  deaf,  and  delirious; 
and  after  another  hour  the  patient  became  stuporous, 
with  cold  feet  and  hands,  and  imperceptible  pulse. 
After  injections  of  strychnine  the  patient  gradually 
recovered,  so  that  within  twelve  hours  after  the  onset 
all  threatening  symptoms  had  passed.  It  was  two  days, 
however,  before  the  patient  was  again  able  to  move 
about  the  room.  Curiously,  guinea-pigs  withstood 
much  larger  doses  of  this  poison  than  ten  drops.  In 
fact,  it  required  I  to  2  cc.  of  the  poison  to  produce 
toxic  symptoms.  The  poison  resisted  heating  to  some 
extent.  Fifteen  minutes'  heating  to  ioo°  C.  did  not 
entirely  destroy  its  toxicity.  The  bacillus,  on  the  other 
hand,  was  easily  killed  at  much  lower  temperatures, 
and  sterilization  of  the  milk  therefore  inhibits  further 
production  of  the  poison. 

According  to  Hoist,70  a  cheese  known  as  "  Knet- 
kase,"  often  produces  attacks  of  acute  gastroenteritis. 
The  cause  of  this  illness  was  found  to  be  a  bacillus 
related  to  the  colon  bacillus.  This  organism  is  very 
highly  virulent  for  rabbits  and  calves,  and  seems  to  be 
similar  to  the  bacillus  of  calf  dysentery,  described  by 
Jensen.  The  cheese  may  become  infected  in  a  number 
of  ways.  The  organism  may  reach  the  cheese  through 
uncleanliness  of  the  persons  engaged  in  its  manufac- 
ture, especially  during  the  kneading  process,  or  during 


82  BACTERIAL   FOOD   POISONING 

the  handling  in  transportation,  or  the  bacillus  may  have 
gotten  into  the  milk  by  being  derived  from  a  cow  suf- 
fering from  some  diarrhceal  infection.  Gaffky,  for 
example,  has  shown  that  diarrhceal  disease  in  man  may 
be  due  to  the  drinking  of  milk  from  a  cow  suffering 
from  diarrhoea. 

Pfliiger 71  described  an  outbreak  of  poisoning  in 
which  intense  colicky  pains,  vomiting,  diarrhoea  with 
great  prostration,  etc.,  developed  suddenly  twelve 
hours  after  the  persons  had  eaten  some  sour  cheese. 
In  some  of  the  cases  there  were  also  disturbances  of 
vision,  diplopia,  dryness  of  the  mouth,  dysphagia,  and 
other  symptoms  resembling  those  of  botulism.  It  is 
possible  that  anaerobic  bacteria  similar  to  the  B.  botu- 
linus  are  concerned  in  this  form  of  cheese  poisoning, 
but  so  far  no  investigations  in  this  direction  have  been 
reported. 

OTHER  BACTERIA  ASSOCIATED  WITH  CHEESE  POISONING. 

In  an  outbreak  of  suspected  cheese  poisoning,  Pep- 
pier 72  isolated  organisms  identical  with  the  bacilli  of 
swine  erysipelas.  According  to  recent  investigations, 
these  bacilli  can  give  rise  to  serious  intestinal  dis- 
turbances in  man.  Furthermore,  tubercle  bacilli  have 
repeatedly  been  found  in  cheese,  though  their  signifi- 
cance in  the  etiology  of  human  infections  is  still  open 
to  question.  According  to  Heim,73  other  pathogenic 
bacteria,  such  as  cholera  or  typhoid,  which  may  chance 
to  get  into  cheese,  usually  die  off  within  a  few  days. 

In  order  to  emphasize  the  importance  of  bacterio- 


POISONING  THROUGH   CHEESE  83 

logical  examinations  in  all  these  poisonings,  the  fol- 
lowing account  of  a  careful  but  disappointing  chemical 
examination  may  not  be  amiss.74  A  piece  of  cheese  to 
which  decided  toxic  symptoms  were  correctly  ascribed 
by  Dr.  Lartigau,  was  sent  to  Professor  Gies  for  exam- 
ination. The  symptoms  were  similar  to  those  given 
by  Vaughan  and  Novy  for  poisonous  cheese.  A  por- 
tion of  the  cheese  was  therefore  extracted  and  ex- 
amined for  tyrotoxicon  by  Vaughan's  method,  with 
negative  results.  A  portion  of  the  extract  was  ex- 
amined for  proteins.  The  greater  portion  of  the  solu- 
ble protein  in  the  extract  was  found  to  consist  of 
deuteroproteose,  with  some  peptone.  After  precipitat- 
ing the  proteose  with  alcohol,  the  filtrate  yielded  on 
evaporation  relatively  large  amounts  of  leucin  and 
tyrosin.  It  also  contained  some  tryptophan.  The  un- 
used residues,  solid  and  liquid,  were  combined  and 
examined  by  the  Stas-Otto  method  for  alkaloidal  sub- 
stances, with  negative  results.  The  authors  conclude 
that  "  in  all  probability  the  poisonous  matter  in  this 
particular  case  consisted  of  toxic  proteose,  although 
this  was  not  suspected  until  practically  all  of  the  ma- 
terial had  been  used  up.  The  seeming  certainty  that 
ptomaines  were  responsible  for  the  symptoms  noted 
had  been  entirely  misleading." 

TREATMENT 

The  treatment  of  these  poisonings  is  entirely  symp- 
tomatic, and  depends  on  the  clinical  type  of  case.  (See 
pages  47  and  71.) 


VI 

POISONING  THROUGH  ICE  CREAM  AND 
PUDDINGS 

HISTORICAL. 

Poisoning  due  to  the  eating  of  vanilla  sauce  or  va- 
nilla ice  cream  is  remarkably  frequent.  The  symptoms 
usually  come  on  within  one  and  one-half  or  two  hours, 
and  consist  in  severe  vomiting,  pains  in  the  stomach 
and  abdomen,  diarrhoea,  and  signs  of  collapse.  At  one 
time  pharmacologists  ascribed  the  poisonous  action  to 
the  vanilla  used  for  flavoring,  but  during  an  outbreak 
of  this  form  of  poisoning  in  1898,  M.  Wassermann  75 
was  able  to  demonstrate  that  a  bacterial  intoxication 
was  involved.  The  poisonous  dish  contained  milk, 
eggs,  sugar,  and  vanilla-sugar  (10  grams  sugar  con- 
taining 20'%  vanilla).  The  dish  was  prepared  in  the 
evening,  and  was  then  kept,  uncovered  and  at  room 
temperature,  in  the  pantry  until  the  following  noon. 
Neither  the  vanilla  nor  the  vanillin  produced  any 
symptoms  when  tested  in  animals.  It  was  found,  how- 
ever, that  vanillin,  the  active  principle  in  the  vanilla 
sugar,  through  its  reducing  action,  favors  the  growth 
of  anaerobic  bacteria.  We  know  that  milk  often  con- 
tains bacteria  which  require  anaerobic  conditions,  are 
pathogenic  for  man,  and  withstand  considerable  heat- 


POISONING  THROUGH    ICE   CREAM  85 

ing.  Under  these  circumstances  we  can  understand 
that  in  the  preparation  of  a  pudding  such  as  that  de- 
scribed, we  have  conditions  altogether  favorable  for 
the  development  of  these  bacteria  and  the  production 
of  their  poisons. 

Vaughan,70  in  studying  an  outbreak  of  poisoning 
due  to  the  eating  of  vanilla  ice  cream,  also  proved  that 
the  vanilla  employed  was  harmless.  The  milk  used 
for  making  the  ice  cream  was  fresh,  and  some  lemon 
ice  cream  made  from  the  same  lot  of  milk  was  abso- 
lutely harmless.  The  custard  mixture  used  for  both 
kinds  of  ice  cream  was  prepared  in  one  lot,  and  then 
divided  into  two  portions.  One  was  flavored  with 
vanilla,  the  other  with  lemon.  According  to  the  in- 
vestigations of  Wassermann,  the  different  behavior 
of  the  two  kinds  of  cream  is  to  be  explained  by  the 
fact  that  vanillin  favors  the  growth  of  anaerobic  bac- 
teria, while  lemon  extract  even  acts  as  an  antiseptic. 

In  studying  an  outbreak  of  poisoning  in  1895,  fol- 
lowing the  eating  of  ice  cream,  Vaughan  isolated  the 
same  colon-like  bacillus  already  mentioned  in  the  out- 
break of  cheese  poisoning. 

BACTERIOLOGY 

In  recent  years  paratyphoid  bacilli  have  been  demon- 
strated as  the  cause  of  poisoning  through  farinaceous 
puddings.  As  already  stated,  Fischer  25  pointed  out 
the  role  played  by  milk  in  spreading  paratyphoid  in- 
fection. In  1904,  Vagedes  "  observed  an  outbreak  of 
poisoning  in  Berlin,  which  he  traced  to  the  eating  of 


86  BACTERIAL  FOOD   POISONING 

farina  pudding.  There  were  seven  cases  in  all,  and 
the  symptoms,  which  came  on  within  a  few  hours  after 
eating  the  pudding,  consisted  of  intestinal  catarrh  ac- 
companied by  fever  and  copious  diarrhoeas.  One  of  the 
cases  ended  fatally,  and  showed  merely  a  distinct 
swelling  of  Peyer's  patches.  The  bacteriological  ex- 
amination of  the  blood-tinged  stools  and  mucus 
showed  the  presence  of  paratyphoid  bacilli  type  B. 
The  same  organism  was  isolated  from  the  spleen,  liver, 
and  kidney  of  the  fatal  case.  In  cultures  this  organ- 
ism produced  a  strong  poison  which  was  quite  resist- 
ant to  heat.  The  serum  of  the  patients  agglutinated 
this  bacillus ;  in  fact,  seven  months  after  the  attack  the 
serum  of  one  of  the  patients  still  showed  agglutinating 
power.  Typhoid  bacilli  were  also  agglutinated  by  the 
serum  of  these  cases,  but  only  in  much  more  concen- 
trated dilutions.  It  was  impossible  to  find  these  para- 
typhoid bacilli  in  the  food  because  nothing  was  left  to 
examine.  Nevertheless  all  the  clinical,  epidemiolog- 
ical, and  bacteriological  data  pointed  strongly  to  the 
farina  pudding  as  the  cause  of  the  poisoning.  The 
pudding  was  prepared  with  farina,  zwieback,  apples, 
milk,  sugar,  vanilla  powder,  and  three  duck  eggs. 
How  the  bacilli  got  into  the  pudding  could  not  be  as- 
certained. It  was  shown  that  neither  the  milk,  vanilla 
powder,  nor  the  zwieback  were  infected.  Perhaps  the 
duck  eggs  were  to  blame,  for  an  examination  of  a  num- 
ber of  other  duck  eggs  shows  that  some  of  them  con- 
tained a  considerable  number  of  bacteria.  It  is  prob- 
able that  decomposed  eggs  may  also  lead  to  poisoning, 


POISONING  THROUGH    ICE   CREAM  87 

for  eggs  constitute  an  admirable  medium  for  the 
growth  of  bacteria,  and  of  course  for  typhoid  and  para- 
typhoid bacilli.  Moreover,  Lange 78  has  pointed  out 
that  bacteria  are  able  to  penetrate  the  intact  shell  and 
so  reach  the  egg  yolk.  Naturally  this  is  still  more 
liable  to  occur  when  the  shell  is  cracked.  It  is  well  to 
bear  in  mind  that  eggs  may  be  the  carriers  of  infection 
in  these  cream  and  pudding  poisonings. 

An  outbreak  of  poisoning  is  reported  by  Cursch- 
mann  2T  in  which  twenty-two  persons  were  taken  ill 
after  eating  a  pudding  composed  of  milk,  eggs,  sugar, 
gelatine  and  vanilla,  and  served  with  raspberry  sauce. 
The  milk  had  previously  been  boiled ;  the  pudding  had 
been  prepared  the  evening  preceding  the  meal,  and  had 
been  kept  in  a  cool  place.  When  eaten  there  was  noth- 
ing whatever  about  taste  or  odor  to  excite  suspicion. 
All  those  who  ate  of  the  pudding  were  attacked  in  five 
to  six  hours  with  severe  abdominal  pains,  vomiting, 
and  diarrhoea;  usually  there  was  also  high  fever  and 
rapid  pulse.  Some  of  the  patients  were  drowsy.  There 
was  no  enlargement  of  the  spleen.  One  of  the  cases 
ended  fatally  in  collapse,  and  came  to  autopsy.  Marked 
inflammatory  changes  were  found  in  the  stomach,  and 
to  some  extent  also  in  the  intestine.  There  was  also 
some  change  in  the  kidney  parenchyma. 

From  the  remains  of  the  pudding,  and  from  the 
stools  of  several  of  the  patients,  as  well  as  from  the 
liver  of  the  fatal  case,  Curschmann  was  able  to  isolate 
a  bacillus  belonging  to  the  enteritidis  group;  this  or- 
ganism was  virulent  for  mice.     It  was  impossible  to 


88  BACTERIAL  FOOD   POISONING 

learn  how  the  bacillus  had  gotten  into  the  pudding, 
or  which  ingredient  had  carried  the  infection.  The 
vanilla  was  free  from  such  bacteria ;  there  was  no  more 
of  the  milk  left  to  examine ;  Curschmann  believed  that 
in  some  unknown  way  the  pudding  had  become  in- 
fected between  the  time  of  making  and  of  eating. 
Since  we  know  practically  nothing  concerning  the  oc- 
currence of  enteritidis  bacilli  in  nature  outside  of  the 
animal  body,  it  is  impossible  to  say  anything  more 
concerning  the  spread  of  such  infections. 

In  1905  Levy  and  Fornet 79  studied  an  outbreak  of 
illness  affecting  seven  persons  in  Strassburg.  The  pa- 
tients were  attacked  with  vomiting  and  severe  diar- 
rhoea, in  some  there  were  also  a  typhoid  roseola  and 
enlargement  of  the  spleen.  The  authors  were  able 
to  isolate  paratyphoid  bacilli,  type  B.,  from  the  stools 
of  all  the  patients.  The  symptoms  appeared  almost 
simultaneously  in  all  the  members  of  the  family,  and 
there  is  no  doubt  that  the  infection  was  due  to  food. 
Investigation  showed  that  only  two  articles  of  food 
could  be  implicated,  namely,  some  liver  sausage  and 
some  vanilla  farina  pudding.  Examination  of  the  liver 
sausage  failed  to  show  any  paratyphoid  bacilli,  and 
there  was  nothing  left  of  the  pudding  to  examine.  Ex- 
amination of  the  farina  itself  and  of  the  vanilla  beans 
yielded  negative  results. 

It  thus  appears  that  the  paratyphoid  bacillus  B. 
plays  an  important  part  not  only  in  meat  poisonings, 
but  also  in  other  food  poisonings.  Thus  far,  however, 
we  have  absolutely  no  information  concerning  the  man- 


POISONING  THROUGH    ICE   CREAM  89 

ner  in  which  the  bacilli  get  into  the  foods.  It  is  sug- 
gestive that  almost  always  the  suspected  foods  have 
contained  milk  and  vanilla.  We  may  recall  that 
Fischer41  in  studying  an  outbreak  of  paratyphoid  in- 
fection in  Futterkamp  found  that  this  was  due  to  the 
drinking  of  milk  from  cows  suffering  from  gastroen- 
teritis. He  also  isolated  the  paratyphoid  bacillus  from 
the  milk  of  these  animals.  In  the  paratyphoid  infec- 
tions associated  with  the  eating  of  farina  puddings, 
we  may  therefore  assume  that  the  milk  was  probably 
the  carrier  of  the  infection.  E.  Klein  80  inoculated 
thirty-nine  specimens  of  milk  into  guinea-pigs,  using 
the  sediment  from  300  cc.  of  milk.  In  ten  of  the 
specimens  the  inoculation  produced  little  foci  of  pus 
in  the  spleen  of  the  animals,  and  further  examination 
revealed  the  presence  of  bacillus  enteritidis  in  these 
foci.  Feeding  a  milk  culture  of  these  bacteria  to 
guinea-pigs  killed  half  of  the  animals  in  five  days.  As 
far  as  could  be  ascertained  none  of  the  cows  yielding 
this  milk  were  ill. 

We  have  already  called  attention  to  the  occurrence 
of  bacilli  of  the  paratyphoid  group  in  the  intestines  of 
normal  animals.  It  is  obvious  that  such  bacilli,  when 
they  are  discharged  in  the  faeces,  especially  about  a 
dairy  barn,  can  quite  readily  find  access  to  the  milk. 
(See  also  Cheese  Poisoning,  page  85.) 

PROPHYLAXIS 

So  far  as  the  prophylaxis  against  this  form  of  food 
poisoning  is  concerned,  very  few  positive  statements 


go  BACTERIAL   FOOD   POISONING 

can  be  made.  Certainly  all  such  puddings,  etc.,  should 
be  thoroughly  boiled,  and,  after  rapid  cooling,  should 
be  eaten  soon  after  cooking.  If  they  are  to  be  kept 
over  for  some  time,  they  should  be  carefully  covered, 
and  then  placed  in  a  cool  place,  preferably  on  ice. 

TREATMENT 

(See  remarks  on  page  83.) 


VII 
POTATO    POISONING 

HISTORICAL 

Large  outbreaks  of  poisoning  through  potatoes  and 
potato  salad  seem  to  be  of  frequent  occurrence  among 
troops.  Schmiedeberg 81  reports  on  an  outbreak  which 
occurred  in  1892,  in  which  357  members  of  one  bat- 
talion were  attacked  with  frontal  headache,  severe 
colicky  pains  in  the  stomach  and  abdomen,  vomiting, 
diarrhoea,  prostration,  and  slight  delirium.  In  a  few 
of  the  cases  the  symptoms  were  quite  threatening, 
cyanosis  of  the  lips,  markedly  dilated  pupils,  syncope, 
rapid  pulse,  etc.  In  the  severe  cases  there  was  some 
rise  in  temperature.  Investigation  pointed  to  new  po- 
tatoes as  the  cause  of  the  outbreak. 

About  the  same  time  a  similar  outbreak  occurred  in 
a  battalion  belonging  to  an  entirely  different  garrison. 
Ninety  men  were  suddenly  attacked  with  frontal  head- 
ache, abdominal  pains,  diarrhoea,  prostration,  and  diz- 
ziness. Some  of  the  patients  had  a  little  rise  in  tem- 
perature, but  none  had  any  dilatation  of  the  pupils 
or  increased  frequency  of  the  pulse.  The  probable 
cause  of  the  outbreak  was  believed  to  be  potatoes. 
Although  somewhat  soft  and  watery,  the  potatoes 
were  generally  quite  ripe. 

91 


92  BACTERIAL   FOOD   POISONING 

In  1893  a  third  outbreak  of  this  form  of  poisoning 
was  reported  from  still  another  garrison,  in  which 
125  men  were  affected  with  symptoms  like  those  just 
enumerated.    All  the  persons  made  a  good  recovery. 

Schmiedeberg  also  cites  an  outbreak  described  by 
Cortial,  occurring  in  Lyons,  in  July,  1888.  This  like- 
wise occurred  among  the  soldiers  and  affected  101 
individuals.  The  main  symptoms  were  prostration, 
colicky  pains,  diarrhoea,  fever,  and  headache.  Some 
of  the  cases  had  dilated  pupils.  The  outbreak  was 
ascribed  to  the  eating  of  potatoes,  both  new  and  old 
sprouting  ones.  After  the  delivery  of  new  potatoes 
was  stopped,  no  more  cases  occurred.  A  dog  that  had 
eaten  three  times  of  these  potatoes  suffered  from  diar- 
rhoea for  a  week.  None  of  the  cases  in  this  outbreak 
ended  fatally. 

In  1898,  E.  Pfuhl 82  reported  an  outbreak  of  poison- 
ing among  some  soldiers.  There  were  fifty-six  cases, 
and  in  almost  all  of  them  the  symptoms  began  a  few 
hours  after  dinner.  Most  of  the  patients  had  chills, 
fever,  headache,  severe  abdominal  pains,  diarrhoea, 
nausea,  drowsiness,  lassitude,  and  some  complained  of 
a  scratchy  feeling  in  the  throat.  The  pupils  were  not 
dilated,  and  the  fever  lasted  only  for  about  three  days, 
dropping  by  crisis.  The  outbreak  was  ascribed  to  the 
eating  of  salted  potatoes. 

SOLANIN  POISONING 

At  one  time  all  these  cases  were  regarded  as  in- 
stances of  solanin  poisoning.    Schmiedeberg,  however, 


POTATO   POISONING  93 

pointed  out  that  this  could  be  accepted  only  when  the 
potatoes  could  be  shown  to  contain  sufficient  solanin 
to  produce  symptoms  of  intoxication.  According  to 
the  investigations  of  Meyer  83  the  solanin  content  of 
potatoes  in  December  and  January  is  0.04  g.  per  kilo 
of  unpeeled  potatoes,  in  March  and  April  it  rises  to 
0.08  to  0.096  g.,  and  in  May,  June  and  July  to  0.100 
to  0.1 16  g.  The  amount  of  solanin,  however,  which 
is  necessary  to  produce  poisoning  is  stated  by  Clarus 
to  be  0.2  to  0.4  g.,  so  that  the  amount  contained  even 
in  a  whole  kilogram  of  potatoes  is  insufficient  to  pro- 
duce the  symptoms  described. 

This  question  has  been  carefully  studied  by  Wint- 
gen.84  In  his  extensive  investigations  he  found  large 
fluctuations  in  the  solanin  content  of  sound  potatoes 
(0.017  to  0.08,  g.  per  kilo),  but  the  quantity  was 
always  small.  When  the  potatoes  were  stored  for  some 
time,  even  when  they  sprouted,  no  increase  in  solanin 
was  observed  provided  the  sprouts  were  carefully  re- 
moved. On  the  other  hand,  in  diseased  potatoes  and 
such  as  are  vigorously  sprouting,  the  solanin  content 
may  be  considerably  higher.  Thus  Meyer  found  0.58 
g.  per  kilo,  in  the  little  dwarf  potatoes  which  had  de- 
veloped from  the  sprouts  of  old  potatoes,  and  in  old 
potatoes  which  were  much  shrunken  and  discolored 
near  the  margins,  he  found  as  high  as  1.34  g.  solanin 
per  kilo.  Wintgen  was  unable  to  discover  any  marked 
difference  in  the  solanin  content  of  sound  and  diseased 
potatoes.  The  distribution  of  solanin  in  the  potatoes  is 
not  at  all  regular;  in  the  peel  the  amount  is  very 


94  BACTERIAL   FOOD   POISONING 

high,  and  toward  the  center  of  the  potato  the  amount 
constantly  decreases.  Weil 85  stated  that  the  quantity 
of  solanin  in  the  potato  increases  under  the  action  of 
bacteria,  and  claimed  to  have  isolated  from  diseased 
potatoes,  two  species  of  bacteria  which  possessed  this 
power.  Wintgen,  however,  was  unable  to  confirm  this 
statement. 

Poisoning  with  potatoes  rich  in  solanin  differs  some- 
what from  poisoning  with  pure  solanin.  In  the  former 
there  are  acute  gastrointestinal  symptoms  and  fever, 
in  addition  to  the  symptoms  observed  in  pure  solanin 
poisoning.  The  reason  for  the  occurrence  of  these 
symptoms  in  the  former  condition  is  because  the  swol- 
len starch  hinders  the  rapid  absorption  of  the  poison, 
giving  the  alkaloid  time  to  reach  the  lower  part  of  the 
intestinal  tract,  where  it  causes  more  or  less  marked 
diarrhoea  in  addition  to  the  vomiting. 

In  the  outbreak  described  by  Pfuhl,82  the  peeled,  raw 
potatoes  contained  0.38  g.  solanin  per  kilo,  and  the 
peeled  boiled  ones,  0.24  g.  The  soldiers  eating  a  large 
portion  (1  kilo)  of  potatoes  thus  took  up  0.30  g.  sola- 
nin, a  quantity  which  is  sufficient  to  produce  consider- 
able toxic  disturbances.  These  quantities  of  solanin, 
however,  are  very  unusual,  and  one  is  not  justified  in 
charging  an  outbreak  of  potato  poisoning  to  the  solanin 
unless  careful  examination  shows  that  the  solanin  con- 
tent was  actually  very  high.  As  a  matter  of  fact,  these 
examinations  have  hardly  ever  been  carried  out. 


POTATO   POISONING  95 

BACTERIA  ASSOCIATED   WITH    POTATO   POISONING 

It  is  extremely  probable  that  bacterial  decomposi- 
tion of  potatoes  by  proteus  bacilli,  an  observation  first 
made  by  Dieudonne,89  is  a  much  more  frequent  cause 
of  potato  poisoning.  During  an  encampment  at  Ham- 
melburg,  in  August,  1903,  150  to  180  soldiers  suddenly 
became  ill  two  hours  after  dinner  with  severe  and  re- 
peated vomiting,  headache,  intense  diarrhoea,  more  or 
less  marked  symptoms  of  collapse,  slight  cramps  in 
the  legs,  etc.  There  was  no  fever.  The  symptoms  be- 
gan to  subside  after  seven  hours,  except  in  a  few  cases, 
where  there  was  slight  delirium,  symptoms  of  collapse, 
and  convulsions.  All  of  the  cases,  however,  recovered. 
The  outbreak  was  ascribed  to  potato  salad,  and  this 
was  accordingly  examined  bacteriologically,  disclosing 
the  presence  of  numerous  proteus  bacilli.  Mice  fed 
with  the  salad  died  in  twenty-four  hours  with  severe 
gastrointestinal  symptoms ;  when  examined  at  autopsy, 
only  a  few  bacilli  were  found  in  the  organs.  Bouillon 
cultures  of  the  bacilli  thus  isolated  were  not  virulent 
for  test  animals ;  but  when  sterile  potatoes  were  inoc- 
ulated with  the  organisms,  and  grown  for  twenty-four 
hours  at  370  C,  a  highly  poisonous  culture  was  ob- 
tained. Mice  fed  with  this  culture  died  in  twenty-four 
to  forty-eight  hours.  If  the  potato  cultures  were  grown 
at  10  to  120  C,  the  resulting  culture  was  unable  to 
kill  mice.  This  shows  that  this  proteus  bacillus  pro- 
duced poisons  on  the  potato,  but  only  at  high  temper- 
atures.   Furthermore,  the  bacillus  was  not  directly  in- 


96  BACTERIAL  FOOD   POISONING 

factious  or  toxic,  but  only  indirectly  through  the  toxic 
substances  produced  from  the  potato. 

It  was  impossible  to  learn  how  the  bacilli  got  into 
the  potatoes,  though  it  was  perhaps  from  the  hands  of 
the  persons  who  did  the  peeling.  The  potatoes  used 
for  the  salad  were  new  and  tender,  but  they  had  been 
boiled  the  night  preceding  the  meal,  then  peeled,  and 
kept  until  the  next  day  in  two  large  baskets  in  a  room 
adjoining  the  camp  kitchen.  The  weather  during  the 
night  and  on  the  next  morning  was  sultry,  a  fact  which 
favored  the  growth  and  development  of  the  germs. 
The  potatoes  used  in  making  the  salad  were  examined 
for  solanin  content,  but  this  was  found  to  be  low, 
0.021  g.  per  kilo.  The  potatoes  did,  however,  contain 
considerable  water,  and  this  favored  their  decomposi- 
tion. 

It  is  interesting  to  know  that  such  poisonings  have 
been  rather  frequent  when  the  potatoes  have  been 
cooked  and  peeled  on  one  day  and  then  kept  in  large 
containers  until  made  into  salad  on  the  next.  In  the 
summer  this  poisonous  decomposition  can  take  place 
with  great  rapidity,  as  is  shown  by  the  following  in- 
teresting outbreak.  In  a  certain  battalion  of  troops 
the  members  of  one  company  became  ill  after  eating 
potato  salad  which  had  been  standing  for  two  hours, 
while  several  other  companies,  two  hours  previously, 
had  eaten  from  the  same  lot  of  salad  without  any 
injurious  effect  whatever.  These  two  hours,  therefore, 
sufficed  for  the  formation  of  the  poisonous  products. 

It  is  very  probable  that  many  of  the  potato  poison- 


POTATO   POISONING  97 

ings  formerly  described  were  not  due  to  solanin,  but 
to  bacterial  decomposition.  As  has  already  been 
pointed  out,  solanin  poisoning  can  only  then  be  as- 
sumed to  have  occurred  when  large  quantities  of  this 
alkaloid  can  be  demonstrated  in  the  potatoes.  Be- 
sides proteus  other  bacterial  infections  are  probably 
carried  by  potatoes.  Both  typhoid  and  paratyphoid 
bacilli  are  known  to  grow  very  well  on  potato.  These 
bacilli  may  get  into  the  potatoes  on  the  farm,  or  the 
potatoes  may  subsequently  be  infected  by  the  infected 
hands  of  a  bacillus  carrier.  In  studying  an  outbreak 
of  potato  poisoning,  therefore,  the  bacteriological  ex- 
amination should  include  a  careful  search  for  typhoid 
and  paratyphoid  bacilli.  The  technique  of  this  exam- 
ination has  already  been  outlined  on  page  38. 

PROPHYLAXIS 

Prophylaxis  against  this  form  of  poisoning  consists 
in  using  the  potatoes  as  soon  as  possible  after  cook- 
ing, and  not  to  keep  them  over  from  one  day  to  the 
next,  especially  in  summer.  Almost  all  the  outbreaks 
of  potato  poisoning  reported  have  occurred  in  July 
and  August,  and  usually  after  the  use  of  new  potatoes. 
Owing  to  their  larger  content  of  water,  these  potatoes 
decompose  much  more  readily  than  old  ones.  In  order 
to  guard  against  solanin  poisoning,  it  is  wise  to  cut  out 
all  sprouts,  and  to  carefully  peel  the  potatoes.  It  is  im- 
portant that  the  kitchen  help  in  all  large  institutions 
(barracks,  hospitals,  hotels,  etc.)  be  frequently  ex- 
amined by  physicians  in  order  to  exclude  bacillus  car- 


98  BACTERIAL  FOOD  POISONING 

riers  from  this  work.  Furthermore,  it  is  essential  to 
insist  on  absolute  cleanliness  on  the  part  of  all  who 
have  the  handling  of  the  food.  Since  the  typhoid  and 
paratyphoid  bacilli  thrive  readily  on  potato,  infection 
with  these  germs,  in  the  way  just  indicated,  may  not 
be  at  all  uncommon. 

TREATMENT 

Treatment  of  potato  poisoning  is  symptomatic,  and 
consists  in  administering  cathartics  and  stimulants,  and 
in  washing  out  the  stomach.    (See  page  47.) 


VIII 
POISONING    THROUGH    CANNED    GOODS 

CANNING    AND    THE    DESTRUCTION    OF    BACTERIA, 

As  the  use  of  canned  goods  becomes  more  and  more 
extensive,  poisonings  of  this  kind  are  increasingly  fre- 
quent. This  is  especially  true  of  canned  meat,  fish,  and 
vegetables.  In  the  process  of  canning,  the  can  with  its 
contents  is  heated  in  an  autoclave  for  one-half  to  one 
hour  at  1120  to  1200  C.  The  cans  are  made  of  thin 
sheet  iron  coated  with  tin.  The  seams  are  pressed, 
and  soldered  with  a  thin  coating  of  solder.  The  cans 
are  filled  with  the  cooked  meat  or  vegetables,  the  cover 
is  put  on  and  then  the  whole  is  sterilized  in  the  auto- 
clave. It  is  true  that  practically  all  bacteria  are  killed 
by  the  temperature  employed,  but  sometimes  the  appa- 
ratus does  not  work  properly,  or  there  is  some  other 
slip,  and  then  bacteria  subsequently  develop.  With 
this,  of  course,  comes  the  development  of  putrefactive 
products.  When  this  is  accompanied  by  the  formation 
of  gas,  the  top  of  the  can  presents  a  convex  appear- 
ance (technically  called  a  "blown"  can),  a  sign  of 
warning  to  the  consumer.  On  opening  such  a  can  a 
foul-smelling  gas  escapes. 

CANNED  MEATS :   CLINICAL  TYPES  OF  CASES 

Poisonings  due  to  canned  meats  have  been  reported 
quite  frequently.    Thus  Bochereau  88  reports  a  number 

99 


ioo  BACTERIAL   FOOD   POISONING 

of  such  instances  occurring  among  the  troops  of  the 
French  army.  The  nature  of  these  is  rendered  very 
probable  by  the  statement  that  of  21,151  cans  examined, 
more  than  fifty  were  more  or  less  "  blown  "  and  de- 
composed. Canned  fish  is  also  frequently  the  cause  of 
poisoning,  and  this  seems  to  occur  especially  with 
canned  salmon,  particularly  when  the  fish  is  not  eaten 
directly  after  the  can  is  opened.  We  have  already 
pointed  that  fish  constitute  a  splendid  medium  for  the 
development  of  bacteria,  and  so  may  easily  become 
the  carriers  of  bacterial  poisons.  The  symptoms  ob- 
served with  poisoning  by  canned  meat  or  fish  are  the 
same  as  have  already  been  described  under  meat  poi- 
soning, and  are  either  gastrointestinal  or  nervous 
(botulism)  in  character. 

An  instance  in  which  canned  pork  and  beans  pro- 
duced three  fatal  cases  of  poisoning  of  the  botulism 
type  has  been  reported  by  Sheppard.97     (See  page  64.) 

CANNED  VEGETABLES 

In  recent  years  a  number  of  outbreaks  of  poisoning 
have  been  reported  following  the  eating  of  canned 
vegetables.  In  Darmstadt,  in  1904,  such  an  instance 
occurred  in  a  cooking  school,  twenty-one  persons  be- 
coming ill  after  eating  bean  salad.  Eleven  of  these 
died.  According  to  A.  Fischer 89  the  symptoms  ap- 
peared twenty-four  to  forty-eight  hours  after  the  meal, 
and  showed  the  typical  characteristics  of  botulism.  (See 
page  64.)  Thus  there  were  disturbances  of  vision, 
ptosis   but   no   mydriasis,    dysphagia,   various   motor 


POISONING  THROUGH   CANNED   GOODS          101 

paralyses,  mostly  bilateral,  increased  frequency  of 
pulse,  etc.  On  the  other  hand,  gastrointestinal  dis- 
turbances, fever,  sensory  and  mental  disturbances  were 
entirely  absent.  Death  occurred  with  symptoms  de- 
noting bulbar  paralysis,  in  two  to  fourteen  days  after 
the  poisoning.  The  autopsy  disclosed  the  usual  signs 
of  asphyxia,  and  hypersemia  and  submucous  hsemor- 
rhages  of  the  lower  part  of  the  intestines.  Otherwise 
there  was  nothing  peculiar.  The  cases  which  recovered 
had  a  very  slow  convalescence.  The  beans  used  for  the 
salad  had  been  canned  by  one  of  the  cooks  of  the  school, 
who  herself  was  one  of  those  poisoned.  On  opening 
the  can  a  peculiar  rancid  odor,  somewhat  resembling 
that  of  Parmesan  cheese,  had  been  noticed,  but  as  there 
were  no  signs  of  decomposition,  nothing  more  was 
thought  of  this.  The  beans  were  very  tender,  "  soft 
as  butter,"  and  were  therefore  not  further  cooked,  the 
salad  being  prepared  after  merely  rinsing  the  beans 
under  the  faucet.  It  was  remarked  that  the  rancid 
odor  increased  after  the  salad  had  stood  a  while.  Only 
those  who  ate  of  the  salad  were  poisoned. 

In  studying  the  cause  of  this  outbreak,  Landmann  90 
examined  some  of  the  salad  left  over,  and  extracted 
this  with  physiological  salt  solution.  After  passing 
the  extract  through  a  Berkfeld  filter  the  sterile  filtrate 
was  found  to  be  highly  toxic,  0.5  cc.  injected  subcu- 
taneously  into  mice  killing  the  animals  with  symptoms 
of  general  paralysis  in  twenty-four  hours.  Boiling 
the  extract  destroyed  the  poison.  This  harmonizes 
well  with  the  fact  that  several  persons  who  ate  some 


102  BACTERIAL  FOOD   POISONING 

of  the  salad  which,  through  an  oversight,  had  been 
placed  on  the  stove  and  allowed  to  boil,  were  not  poi- 
soned. So  also  in  another  case,  where  some  of  the 
salad  was  eaten  after  moderate  heating ;  the  toxic  symp- 
toms developed  very  slowly,  with,  however,  a  fatal 
ending.  Bacteriological  examination  of  the  salad  re- 
vealed the  presence  of  an  anaerobic  bacillus  which  was 
identical  with  bacillus  botulinus.  This  organism  pro- 
duced a  strong  poison  in  cultures,  especially  when 
grown  at  240  C,  so  that  white  mice  were  killed  with 
O.000003  cc.  and  guinea-pigs  with  0.0003.  When 
grown  at  370  C,  on  the  other  hand,  the  fatal  dose  for 
mice  was  0.01  cc,  and  for  guinea-pigs  0.1  cc.  Gaffky 
also  isolated  the  bacillus  botulinus  from  this  salad. 

It  was  impossible  to  learn  how  the  string  beans  had 
become  infected.  Landmann  believed  that  the  bacilli 
had  been  carried  into  the  can  along  with  some  little 
piece  of  left-over  meat  such  as  might  readily  be  found 
in  any  kitchen.  He  bases  this  view  on  the  fact  that 
thus  far  the  bacillus  botulinus  has  been  found  only  in 
meats  or  dishes  prepared  from  meat.  It  is  also  possible, 
however,  that  the  spores  of  this  bacillus  were  carried 
in  on  the  beans  from  the  field.  In  the  canning  as 
carried  out  in  the  cooking  school  the  sterilization  ap- 
pears to  have  been  incomplete;  it  is  probable  that  in  a 
regular  canning  factory  where  sterilization  is  carried 
out  at  1120  C,  all  of  the  spores  would  have  been 
killed.  It  follows  from  what  has  been  said  that  canned 
vegetables  having  the  least  rancid  odor  should  be  de- 
stroyed, and  that  even  those  appearing  normal  in  every 


POISONING  THROUGH    CANNED   GOODS  103 

way  should  always  be  boiled  before  serving.  If  this 
had  been  done  in  the  case  just  described,  the  catas- 
trophe would  have  been  averted. 

An  extensive  outbreak  of  poisoning  due  to  the  eat- 
ing of  string  beans  occurred  in  Leipzig  in  1906,  among 
the  employees  of  a  large  department  store.  About  250 
persons  were  affected,  a  few  hours  after  the  meal,  the 
chief  symptoms  being  abdominal  pains,  chills,  nausea, 
headache,  and  dizziness.  In  some  of  the  patients  the 
symptoms  were  at  once  accompanied  by  diarrhoea;  in 
others  the  diarrhoea  came  on  during  the  evening  or  the 
following  morning.  The  symptoms  lasted  two  to  four 
days,  all  the  cases  making  a  good  recovery.  The 
string  beans  were  delicious,  and  showed  nothing  ab- 
normal in  taste  or  odor.  They  had  been  packed  in  sev- 
eral cans,  which  had  been  opened  just  before  the  meal, 
and  then  placed  for  a  time  in  hot  water  (about  80 °  C). 
Boiling  was  purposely  omitted  because  the  beans  were 
so  tender  that  they  would  have  made  a  soft  mush.  The 
bacteriological  examination  made  by  Roily 91  disclosed 
the  presence  of  two  species  of  bacteria,  bacillus  coli,  and 
bacillus  paratyphi,  type  B,  both  in  large  numbers.  No 
anaerobic  organisms  were  isolated.  The  paratyphoid 
bacilli  were  pathogenic  for  mice  and  guinea-pigs  when 
inoculated  subcutaneously ;  in  cultures  the  bacilli  pro- 
duced a  toxin  which  was  resistant  to  heat.  The  poi- 
soning in  his  case  was  due  to  the  toxin  and  not  to  the 
bacteria  themselves,  for  otherwise  the  symptoms  would 
not  have  appeared  so  suddenly,  but  would  have  re- 
quired a  period  of  incubation.    Furthermore,  in  none 


104  BACTERIAL   FOOD   POISONING 

of  the  cases  could  paratyphoid  bacilli  be  found  in  the 
stools. 

LINICAL  TYPES  OF  CASES, 

We  see,  then,  that  in  poisoning  due  to  canned  vege- 
tables the  same  two  types  of  bacteria  occur  as  are  found 
in  outbreaks  of  meat  poisoning,  namely,  bacillus  botu- 
linus,  which  produces  a  poison  readily  decomposed  by 
heat,  and  bacillus  paratyphi,  B,  whose  poison  with- 
stands heating.  The  first  variety  of  poisoning  can  be 
guarded  against  by  heating  the  food  to  boiling  just 
before  serving,  although  it  is  better  not  to  eat  any  food 
about  whose  condition  there  is  the  least  question. 
The  second  variety  of  poisoning  cannot  be  safeguarded 
against  even  by  prolonged  boiling. 

Belser  92  made  careful  bacteriological  examinations 
of  canned  vegetables  which  had  undergone  decompo- 
sition, as  was  shown  by  the  ballooned  tops  of  the  cans. 
He  found  that  the  change  was  due  to  a  number  of 
bacteria  which  were  more  or  less  resistant  to  heat,  such 
as  bacillus  acidi  lactici,  and  bacillus  amylobacter.  In 
almost  every  case  the  decomposed  vegetables  showed 
an  increased  acidity,  though  sometimes  this  was  but 
slight.  The  bacilli  were  not  virulent  for  mice.  Ba- 
cillus proteus  was  also  encountered;  this  organism 
grows  especially  well  in  the  broth  of  peas  and  beans, 
and  produces  a  toxin  highly  virulent  for  mice.  Bac- 
teria ordinarily  occurring  in  water  and  soil  have  also 
been  found  in  canned  vegetables ;  among  these  are  ba- 
cillus mesentericus  vulgatus,  and  bacillus  megatherium. 


POISONING  THROUGH    CANNED   GOODS  105 

BACTERIOLOGICAL   EXAMINATION 

It  is  impossible  to  determine  the  absolute  sterility  of 
canned  goods  without  a  careful  bacteriological  ex- 
amination. According  to  E.  Pfuhl,8T  canned  goods 
often  contain  bacteria  without  showing  any  ballooning 
of  the  top.  The  reason  for  this  is  that  the  bacteria  in- 
fecting the  can  do  not  all  produce  gas.  Furthermore, 
the  appearance  of  the  contents  on  opening  the  can  may 
also  give  no  hint  of  the  presence  of  bacteria.  Fre- 
quently all  that  is  noticed  is  that  the  contents  have  a 
slightly  sour  odor,  or  one  abnormally  pungent.  Where 
large  purchases  are  made,  it  is  therefore  necessary  al- 
ways to  have  several  cans,  selected  at  random,  exam- 
ined bacteriologically.  The  goods  should  not  be  ac- 
cepted if  this  examination  discloses  the  presence  of  any 
bacteria.  Pfuhl  gives  the  following  method  to  be  fol- 
lowed in  making  the  examination:  The  can  is  kept 
unopened  in  the  incubator  for  eight  to  fourteen  days. 
This  gives  the  obligate  and  faculative  anaerobic  bacteria 
opportunity  to  develop.  Then  the  lid  is  carefully  ster- 
ilized by  flaming  with  alcohol,  and  a  hole  made  with  a 
sterile  ice  pick  or  other  sharp  instrument.  Through 
this  hole  some  of  the  meat  juice  and  liquefied  gelatine 
is  sucked  up  with  a  sterile  pipette  and  planted  into  dif- 
ferent media  both  for  aerobic  and  anaerobic  growth. 
The  hole  is  then  covered  with  a  bit  of  sterile  cotton, 
and  the  can  returned  to  the  incubator  for  another  two 
or  three  days.  This  gives  the  aerobic  bacteria  time  to 
develop.     Then  another  set  of  cultures  is  made.    The 


106  BACTERIAL  FOOD  POISONING 

second  test  may  be  omitted  if  bacteria  develop  with 
the  first  test. 

PROPHYLAXIS 

Schottelius 83  has  repeatedly  warned  against  the 
ever-increasing  use  of  canned  foods  in  the  household, 
and  we  believe  the  warning  fully  justified.  There  is 
a  distinct  field  of  usefulness  for  this  form  of  food,  for 
example,  in  the  feeding  of  armies  in  war,  or  in  expe- 
ditions of  various  kinds.  On  the  other  hand,  in  tem- 
perate climates,  as  for  example  in  Germany  or  in  the 
United  States,  there  is  really  no  reason,  aside  from  con- 
venience, why  canned  foods  should  be  used  in  the 
household.  It  seems  not  to  be  appreciated  that  canned 
goods  are  always  inferior  to  fresh  vegetables,  fruits, 
etc.*  Furthermore,  just  the  fact  that  certain  fruits  or 
vegetables  are  out  of  season  for  part  of  the  time  each 
year,  makes  our  appetite  and  appreciation  of  them  all 
the  keener  when  the  season  returns.  If  we  had  straw- 
berries and  cream  every  day  of  the  year,  we  should 
soon  be  disgusted  by  the  mere  sight  of  them.  Another 
disquieting  fact  is  that  at  the  present  time  we  have  no 
way  of  determining  the  age  of  the  goods  we  are  buy- 
ing. It  will  be  recalled  that  the  proposal  to  date  all 
canned  goods  met  with  determined  opposition  on  the 

♦While  the  superiority  of  fresh  foods  is  unquestioned, 
there  is  probably  very  little  danger  of  food  poisoning  from 
fruits  or  vegetables  properly  canned  by  a  reputable  firm. 
In  fact,  it  is  likely  that  the  "  canning "  as  done  in  such  an 
establishment  (in  steam  sterilizers  under  pressure),  is  more 
efficacious  than  that  done  at  home. 


POISONING  THROUGH   CANNED   GOODS          107 

part  of  the  large  packers.  Yet  there  is  no  doubt  what- 
ever that  the  danger  of  decomposition  increases  with 
age,  and  there  is  also  a  loss  of  flavor.  Under  no  cir- 
cumstances should  the  contents  of  a  "  blown  "  can  be 
eaten.  It  is  said  that  unscrupulous  packers  have  taken 
"  blown "  cans  which  had  been  returned  to  them, 
punched  a  small  hole  in  the  cover  to  let  out  the  gas, 
reheated  the  whole  in  the  autoclave,  resoldered  the 
punch  hole,  and  then  resold  such  goods  at  a  reduced 
price.  It  will  be  well,  therefore,  to  refuse  canned 
goods  showing  more  than  one  soldered  opening. 

TREATMENT 

(See  pages  47  and  71.) 


IX 
METALLIC    POISONS 

HISTORICAL 

There  is  still  a  widespread  belief  among  the  laity 
that  epidemic  outbreaks  of  food  poisoning  are  often 
due  to  metallic  poisons.  As  a  matter  of  fact,  this  is 
rarely  the  case.  Nevertheless,  notable  outbreaks  of 
this  nature  have  been  known  even  in  recent  years. 
Thus  the  famous  "  beer  epidemic  "  of  Manchester  and 
other  English  cities,  in  1900,  was  due  to  the  accidental 
presence  of  arsenic.  At  one  time,  too,  the  chief  cause 
of  poisoning  through  canned  foods  was  thought  to  be 
metallic  poisons,  especially  lead  and  tin,  but  K.  B. 
Lehmann  94  declares  that  this  is  not  true  at  the  present 
time.  In  Germany  the  law  prescribes  that  the  tin  used 
for  tinning  the  cans  shall  not  contain  over  1%  lead, 
and  the  solder  not  over  10%.  Lead  poisoning  from 
this  source  is  unknown  in  that  country  since  the  enact- 
ment of  this  law.  Poisoning  from  tin  is  probably  also 
very  infrequent.  According  to  Lehmann  acute  diges- 
tive disturbances  may  be  caused  by  foods  which  con- 
tain large  amounts  of  tin  (100  to  several  hundred 
milligrams),  but  the  symptoms  are  usually  not  severe. 
Freshly  canned  goods  contain  but  little  tin;  the 
amount,  however,  gradually  increases  in  time,  so  that 

108 


METALLIC    POISONS  109 

canned  vegetables  were  found  with  from  fifty  or  sixty 
mg.  to  200  mg.  per  kilo.  Canned  meats  contained  all 
the  way  from  fifty  to  325  mg.  The  largest  amounts 
were  found  in  decomposed  canned  foods,  for  in  these 
the  acid  which  was  formed  in  the  decomposition  dis- 
solved the  tin.  Large  amounts  were  also  found  in 
acid  preserves,  such  as  pickled  herring.  In  one  such 
instance  156  mg.  of  tin  were  found  in  150  grams  of  the 
pickled  fish.  It  is  important,  therefore,  to  insist  that 
preserves  containing  considerable  quantities  of  acetic, 
tartaric,  or  malic  acid  be  packed  only  in  glass  or  por- 
celain, and  not  in  tin. 

According  to  Lehmann  the  ordinary  vegetable  or 
meat  preserves,  which  are  not  highly  acid,  do  not  ap- 
pear to  give  rise  to  any  metallic  poisoning.  What 
poisoning  does  occur  is  almost  always  of  bacterial 
origin. 

Copper  poisoning  was  also  formerly  believed  to  play 
an  important  role  in  food  poisoning.  Lehmann96 
states  that  about  200  mg.  copper  must  be  swallowed  be- 
fore symptoms  are  produced  in  man,  and  1200  mg.  are 
needed  to  produce  really  threatening  symptoms.  It 
is  difficult  to  see  how  such  quantities  of  copper  could 
be  present  in  the  food  under  ordinary  conditions,  and 
there  is  little  doubt  that  most  of  the  poisonings  ascribed 
to  verdigris  and  copper  are  really  due  to  bacterial  de- 
composition of  the  food.  In  fact,  the  symptoms  re- 
ported in  these  cases  are  very  much  like  those  of  the 
latter  condition. 

There  is  reason  to  believe  that  under  certain  condi- 


110  BACTERIAL   FOOD   POISONING 

tions,  lead  poisoning  may  occur  quite  readily.     Thus 
earthen  ware  is  sometimes  coated  with  a  cheap  glaze 
containing  large  quantities  of  lead.    On  boiling  fluids 
containing  vinegar  in  such  pots,  considerable  amounts 
of  lead  pass  into  solution.    Thus,  in  some  tests  made  in 
this  direction,  ioo  to  700  mg.  lead  were  extracted  with 
the  first  boiling.     Lehmann96  believes  that  attention 
should  be  directed  to  this  pottery,  because  the  lead  is 
given  off  for  a  long  time.     Perhaps  these  lead  glazes 
are  responsible  for  some  hitherto  unexplained  cases  of 
lead  poisoning.    Lehmann  cites  a  case  of  lead  poison- 
ing observed  by  Halenke.     Two  women  had  cooked 
cranberries  in  an  earthen  pot,  and  had  then  made  a 
cranberry  tart.     Soon  after  eating  the  tart  both  be- 
came ill,  one  very  severely.    Investigation  showed  that 
the  glaze  had  been  completely  dissolved  from  the  inside 
of  the  pot,  and  that  a  piece  of  tart  contained  about  160 
mg.  lead.    Each  woman  had  therefore  consumed  about 
400  to  600  mg.  lead  in  the  form  of  lead  malate.    Ap- 
proximately 1000  mg.  lead  had  been  given  off  by  the 
glaze  in  the  one  boiling.    It  will  be  well,  when  investi- 
gating chronic  lead  poisonings  whose  origin  cannot  be 
traced,  to  think  of  cheap  pottery  with  a  lead  glaze.  The 
determination  of  the  lead  content  can  easily  be  under- 
taken by  any  physician  by  merely  boiling  the  pot  with 
4%  acetic  acid  for  half  an  hour,  and  then  passing  sul- 
phureted  hydrogen  through  the  fluid.     A  black  dis- 
coloration or  a  black  precipitate  denotes  the  presence 
of  lead. 

It  is  well  to  remember,  however,  that  metallic  poi- 


METALLIC    POISONS  in 

sonings  through  cooking  utensils,  etc.,  are  quite  rare, 
and  one  is  justified  in  ascribing  poisoning  to  this  cause 
only  if  a  chemical  examination  has  really  demonstrated 
large  quantities  of  such  a  poison.  The  mere  fact  that 
the  food  was  prepared,  for  example,  in  a  damaged  cop- 
per vessel,  by  no  means  justifies  the  diagnosis  of  cop- 
per poisoning.  In  fact,  one  should  first  think  of  bac- 
terial poisoning,  for  this  is  much  more  likely  to  have 
occurred. 


BIBLIOGRAPHY 


BIBLIOGRAPHY 

GENERAL    ARTICLES 

Novy,  F.  G. — Article  on  Food  Poisons,  in  Modem  Med- 
icine, Osier,  Vol.  I.,  1907. 

Vaughan  and  Novy. — "  Cellular  Toxins,"  Fourth  Edi- 
tion, N.  Y.,  1902. 

Vaughan,  V.  C. — "  Protein  Poisons,"  Science,  N.  Y., 
1907. 

Thresh  and  Porter. — "  Preservatives  and  Food  Exam- 
ination/' Blakiston's  Son  &  Co.,  Phila.,  1906. 

MEAT     POISONINGS 

1.  Bollinger. — Arztl.  Intelligenzblatt.  Milnchener  med. 

Wochenschr.,  Vol.  28,  1881. 

2.  Ostertag. — Handbuch  der  Fleischbeschau.    4.  Aufl. 

1902.  (Review  of  the  older  literature.)     There  is 
an  English  translation  of  this. 

3.  van     Ermengem. — Handbuch     von     Kolle-W  asser- 

mann.    Vol.  2,  1903. 

4.  Schneidemuhl. — Die  animalischen  Nahrungsmittel, 

1903.  (Review  of  the  older  literature.) 

5.  Gartner. — Korresp.-Blatt    des    arztl.    Vereins    von 

Thiiringen,  1888. 

6.  Gaffky  und  Paak. — Arb.  a.  K.  Gesnndh.  A.,  Vol. 

6,  1890. 

"5 


Ii6  BACTERIAL   FOOD   POISONING 

7.  Neelson,  Johne  und  Gartner. — Cited  by  Ostertag 

(2). 

8.  Van  Ermengem. — 'Bull.  acad.  de  med.  de  Belgique, 

1892. 

9.  Holst. — Ref.  Centralblatt  f.  Bakter.,  Vol.  17,  1895. 

10.  Poels  und  Dhont. — Holland.  Zeitschr.  f.  Tierheil- 

kunde,  Vol.  24,  1894. 

11.  Basenau. — Archiv.  f.  Hyg.,  Vol.  20,  and  Vol.  32. 

12.  Fischer,  B. — Zeitschr.  f.  Hyg.,  Vol.  39,  1902.  (Re- 

view of  literature.) 

13.  Johne. — Cited  by  Ostertag,  Handbuch  der  Fleisch- 

beschau  (2). 

14.  Van  Ermengem. — Revue  d'hyg.,  1896. 

15.  Kaensche. — Zeitschr.  f.  Hyg.,  Vol.  22,  1896. 

16.  Scheef. — Med.  Korrespondenzblatt  des  Wurtt.  arztl. 

Landesvereins,  1896. 

17.  Gijnther. — Arch.  f.  Hyg.,  Vol.  28,  1896. 

18.  Silberschmidt. — Korrespondenzblatt  fur  Schweizer 

Arztl,  1896. 

19.  Pouchet. — Annates  d' Hygiene,  1897. 

20.  Durham. — British  med.  Journal,  1898,  1899. 

21.  De  Noble. — Ann.  soc.  med.  Gand.,  1899,  1901. 

22.  Hermann  and  Van  Ermengem. — Arch,  de  medic. 

ex  per.,  1899. 

23.  Trautmann. — Zeitschr.  f.  Hyg.,  Vol.  45,  1903. 

24.  Van  Drigalski. — Festschrift  fur  R.  Koch.     Jena, 

1903. 

25.  Fischer,  B. — Ibid. 

25a.  Muhlens,  Dahm,  and  Furst. — Abstracted  in  Jour- 
nal of  the  Royal  Institute  of  Public  Health,  Vol. 
XVI,   1908. 

26.  Uhlenhuth. — Gedenkschrift  fur  Leuthold.    Berlin, 

1906. 


BIBLIOGRAPHY  117 

27.  Curschmann. — Zeitschr.   f.   Hyg.,   Vol.   55,    1906. 

(Review  of  recent  literature.) 

28.  Kutscher. — Ibid. 

29.  Heller. — Centralbl.  f.  Bakt.  Orig.,  Vol.  43. 

30.  Fromme. — Ibid. 

31.  Schottmuller. — Deutsche  med.  Wochenschr.,  1900. 

Zeitschr.  f.  Hyg.,  Vol.  36,  1901. 

32.  Durham. — The  Lancet,  1898. 

2,Z-  Trautmann. — Zeitschr.  f.  Hyg.,  Vol.  46,  1904. 

34.  Kayser. — Centralbl.    f.    Bakt.,    Vol.    35,    1903.     v. 

Krehl  imd  Kayser,,  Deutsche  med.  Wochenschr., 
1906. 

35.  Hetsch. — Klin.  Jahrbuch.,  Vol.  16,  1906. 

36.  Rolly. — Deutsches  Arch.  f.  klin.  Medizin.,  Vol.  87, 

1906. 
2,y.  Zupnik. — Zeitschr.  f.  Hyg.,  Vol.  40. 

38.  Kutscher. — Paratyphus      in:       Kolle-Wassermann 

Handbuch.     1.  Erg'dnzungsband,  1907. 

39.  Levy  und  Jakobstal. — Arch.  f.  Hyg.,  Vol.  44,  1903. 

40.  Pies. — Archiv  f.  Hyg.,  Vol.  62,  1907. 

41.  Fischer,  B. — Zeitschr.  f.  Hyg.,  Vol.  39,  and  Fest- 

schrift fur  R.  Koch. 

42.  Uhlenhuth. — Deutsche  med.  Wochenschr.,  Nr.  11, 

1907. 

43.  Basenau. — Arch.  f.  Hygiene,  Vol.  32,  1898. 

44.  Levy. — Arch.  f.  experiment.  Pathol,  1894;  Vol.  34. 

45.  Wesenberg. — Zeitschr.  f.  Hyg.,  Vol.  28,  1898. 

46.  Glucksmann. — Centralbl.  f.  Bakt.,  Vol.  25,  1899. 

47.  Silberschmidt. — Zeitschr.  f.  Hyg.,  Vol.  30,  1899. 

48.  Pfuhl,  A. — Zeitschr.  f.  Hyg.,  Vol.  35,  1900. 

49.  Schumburg. — Zeitschr.  f.  Hyg.,  Vol.  41,  1902. 

50.  Lubenau. — Centralbl.  f.  Bakt.  Orig.,  Vol.  40,  1906. 


n8  BACTERIAL   FOOD   POISONING 

51.  Van  Ermengem. — Zeitschr.  f.  Hyg.,  Vol.  26,  1897; 

and   Kolle-Wassermann,   Handbuch  d.   pathog. 
Mikroor ganismen,  Vol.  2. 

52.  Kempner. — Zeitschr.  f.  Hyg.,  Vol.  26,  1897. 

53.  Roemer. — Centralbl.  f.  Bakt.,  Vol.  27,  1900. 

54.  Schilling. — Deutsche  med.   Wochenschr.,  1900. 

55.  Bryson,    M. — British   Medical   Journal,    1907,    II., 

page  1710. 

56.  Brown,  G.  A. — Lancet,  1907,  I.,  page  1029. 

56*.  Pennington,  Mary  E. — Yearbook,   U.  S.  Depart- 
ment of  Agriculture,  1907. 

57.  Morgan,  H.  deR. — British  Medical  Journal,  1905,  I., 

page  1257. 

58.  Liefmann,  H. — Munchener  medizin.  Wochenschrift, 

Vol.  55,  1908,  page  157. 

59.  Ohlmacher. — Journal  Medical  Research,  1902,  Vol. 

VII.,  page  411. 

60.  Owen,   R. — The  Physician  and  Surgeon,   Detroit, 

1907,  Vol.  29,  page  289. 

61.  Hubener. — Deutsche  med.  Wochenschrift,  1908,  No. 

24. 

62.  Rimpau,  W. — Ibid. 

62a.  Berry,  W. — Public  Health,  Vol.  XXII,  1908,  page 

FISH     POISONINGS 

6^.  Kobert. — Uber  GiftHsche  und  Fischgifte,  Stuttgart, 
1905. 

64.  Ulrich. — Zeitschr.  f.  Hyg.,  Vol.  53,  1906. 

65.  Abraham. — Munch,   med.    Wochenschr.,    1906,   Nr. 

50,  Vol.  2466. 

66.  Galeotti  und  Zardo. — Centralbl.  f.  Bakt.  Orig.,  Vol. 

31,  1902. 


BIBLIOGRAPHY  119 

67.  Vivaldi  and  Rodella. — Hygien.  Rundschau,  1905. 

68.  Vagedes. — Vierteljahrschr.    f.    gerichtl.    Medizin., 

Vol.  30.  I905- 

CHEESE    POISONING 

69.  Vaughan  and  Perkins.— Arch.  f.  'Hyg.,  Vol.  27, 

1896. 

70.  Holst,  A.— Centralbl.  f.  Baku,  Vol.  20,  1896. 

71.  Pfluger. — Zeitschr.  f.  Medizinalbeamte,  1894. 

72.  Peppler.— Cited  by  Heim,  Lehrbuch  der  Hygiene, 

page  26,  1903. 

73.  Heim. — Arb.  aus  dem  K.  Gesundheitsamt.,  Vol.  5. 

74.  Taltavall  and  Gies.— New  York  Medical  Journal, 

1907,  Vol.  86,  726. 

poisonings  through  ice  cream  and  puddings 

75.  Wassermann,    M.— Zeitschr.    f.    diatei.    u.    phys. 

Therapie.,  Vol.  3,  1896. 

76.  Vaughan.— Arch.  f.  Hyg.,  Vol.  7. 

yy.  Vagedes. — Klin.  Jahrbuch.,  Vol.  14,  1905. 

78.  Lange.— Arch.  f.  Hygiene,  Vol.  62,  H.  3. 

79.  Levy  und  Fornet.— Centralbl.  f.  Bakt.  Orig.,  Vol. 

41,  1906. 

80.  Klein,  E.— Centralbl.  f.  Bakt.  Orig.,  Vol.  38,  1905. 

POTATO     POISONINGS 

81.  Schmiedeberg.— Arch.     f.     exper.     Pathologie    u. 

Pharm.,  Vol.  36,  1895. 

82.  Pfuhl,  E. — Deutsche  med.  Wochenschr.,  1899. 

83.  Meyer.— Arch.  f.  exper.  Path.  u.  Pharm.,  Vol.  36, 

1895. 


120  BACTERIAL  FOOD   POISONING 

84.  Wintgen. — Zeitschr.   fur    Untersuchung   der  Nah- 

rungs-  und  Genussmittel.,  Vol.  12,  1906. 

85.  Weil. — Arch.  f.  Hyg.,  Vol.  38,  1900. 

86.  Dieudonne. — Deutsche  militararztl.  Zeitschr.,  1904. 

POISONINGS    THROUGH     CANNED    GOODS 

87.  Pfuhl,  E. — Zeitschr.  f.  Hygiene.,  Vol.  48,  1904. 

88.  Cited    by    Bischoff    und    Wintgen. — Zeitschr.    f. 

Hyg.,  Vol.  34,  1900. 

89.  Fischer,  A. — Zeitschr.  f.  klin.  Medizin.,  Vol.   59, 

1906. 

90.  Landmann. — Hygien.  Rundschau.,  Vol.  14,  1904. 

91.  Rolly. — Munch,  med.  Wochenschr.,  1906. 

92.  Belser. — Arch.  f.  Hyg.,  Vol.  54,  1905. 

93.  Schottelius. — Blatter    filr    VolksgesundheitspHege, 

Vol.  7,  1907. 

94.  Lehmann. — Arch.  f.  Hyg.,  Vol.  45,  1902. 

95.  Lehmann. — Deutsche  Vierteljahrsschr.  f.  offentlliche 

Gesundheitspiiege,  Vol.  34,  1902. 

96.  Lehmann. — Hygienische  Rundschau.,  1902. 

97.  Sheppard,     C. — Southern    California    Practitioner, 

1907,  Vol.  22,  page  370. 


INDEX 

PAGE 

Abraham,  studies  on  fish  poisoning •.•••: 74 

Abscesses  in  meat,  their  relation  to  meat  poisoning 24 

Acids  of  fruits,  in  relation  to  canned  goods 109 

Aertryck,   bacillus   of 3°>   74 

outbreak  of  food  poisoning  in...._. 3° 

Agglutination  reaction  in  food  poisoning. ._ 24,  40,  45,  73,  74 

Alcohol,  clinical  application  in  food  poisoning 18,  47 

Allantiasis 62 

Alsfeld,  outbreak  of  food  poisoning  _  in. . 3° 

Andelfinger,  outbreak  of  meat  poisoning  in 17 

Antitoxin    for    botulism 68,  71 

Arsenic,  cause  of  beer  epidemic 108 


Bacillus  acidi  lactici  in  canned  vegetables 104 

Bacillus  Aertryck,  occurrence  in  fish  poisoning 74 

occurrence    in   healthy    animals 33 

amylobacter    104 

botulinus     62,  67,  101 

growth  as  affected  by  salt 7° 

growth   in    symbiosis 69 

bovis   morbificans 27 

carriers    31,  34 

coli  in  canned  vegetables 103 

in  cheese  poisoning 81 

in  meat  poisoning 48,  54 

in   oysters    78 

toxin  of   48 

enteritidis,   Gartner  agglutination   of 24 

biological    characteristics    35 

in   meat    poisoning 40,    54 

in   pudding    87 

occurrence   in  nature 31,   34 

relation  to  other  organisms 26 

of  calf  dysentery,  in  cheese  poisoning 81 

of  hemorrhagic  septicaemia 77 

of    swine    erysipelas 82 

of  tuberculosis  in  cheese 82 

paratyphi,   biological    characteristics 35 

in    canned    goods 103 

in  ice  cream  and  pudding  poisonings 85,  86,  88 

occurrence _  in  nature 31,  33,   34,  73,  74 

pathogenicity    37 

peptonificans,   in   meat   poisoning 55 

121 


122  INDEX 

_      .„                                  .  PAGE 

Bacillus  proteus,  action  of 51 

in  blown  cans 48,    104 

in   meat   poisoning 48,    50,   51,    52 

in    mussel    poisoning 78 

in   oysters    78 

in  potato   poisoning 95 

pathogenicity    52 

toxin  of  49,  51,  95 

subtilis,    in   meat   poisoning 54,  69 

suipestifer,  occurrence  in  nature 33 

typhi,   biological   characteristics 35 

in   oysters    78 

viability    in    cheese 82 

Bacteria  in  bile  of  slaughtered  animals 32 

Bacteriological  examination,  of  canned  goods,  technique. . .  105 

of  meat,   technique 38 

Barbs    (poisonous  fish) 72 

Basenau,  studies  on  meat  poisoning 27 

technique  of  bacteriological  examination 38 

Beelitz,  outbreak  of  meat  poisoning  in 54 

Beer  epidemic,   in   England 108 

Belser,  bacteriology  of  blown  cans 104 

Berlin,   outbreak   of  meat  poisoning 30 

Bern,  outbreak  of  meat  poisoning 30 

Berry,  studies  on  meat  poisoning 54 

Bischofswerde,  outbreak  of  meat  poisoning  in 28 

"Blown  cans,"  bacteria  associated  with 104 

as    evidence   of   putrefaction 99,  106 

Bollinger,  studies  on  meat  poisoning 15,  16 

Botulism,    antitoxin    for 68 

diagnosis      70 

etiology    62,  66 

mortality   in    64 

prophylaxis     70 

symptoms    64,  65 

treatment     71 

Boucherau,  poisoning  through  canned  goods 99 

"  Braxy,"  relation  to  meat  poisoning 21 

Breslau,  outbreak  of  meat  poisoning  in 30 

Brieger,  studies  on  mussel  poisoning 76 

Brown,  G.  A.,  studies  on  meat  poisoning 24 

Brown,  H.  R.,  cold  storage  of  poultry 58 

Brugge,  outbreak  of  meat  poisoning  in 30 

Canned  beans,  bacillus  botulinus  in 101 

goods,  poisoning  through,  clinical  types 104 

poisoning    through,    etiology 99 

poisoning    through,    prophylaxis 106 

vegetables,  bacteria  associated  with  poisoning  from..ioi,  103 

Cans,  "  blown  "   99>  106 

Carriers  of  typhoid  and  other  bacilli 31 

Chadderton,   outbreak  of  meat  poisoning  in 30 


INDEX  123 

PAGE 

Chemnitz,  outbreak  of  meat  poisoning  in 50 

Cheese  poisoning,  bacteria  associated  with 80,  82 

chemical   examination   of 83 

clinical  types 80 

treatment ■ 83 

Cholera  nostras,  due  to  paratyphoid  bacilli 43 

spirilla,  in  cheese,  viability  of 82 

spread    by    oysters 78 

Cold-storage    poultry    in    meat    poisoning 57 

influence    of,    on   bacterial    multiplication 57,58 

Colon  bacillus  in  meat  poisoning 48-  54 

in  oysters    78 

in  canned  vegetables i°3 

in    cheese    poisoning 81 

toxin  of    48 

Communicability  of  epidemic  meat  poisoning 19,  24,  29,  44 

Cooking,  effect  on  bacterial  poisons 21,  27,  51,  54,  67,  74,  104 

Copper,   in   food   poisoning 109 

Cortial,  on  potato  poisoning 92 

Cotta,  outbreak  of  meat  poisoning. .  . . 25 

Curschmann,  poisoning  due  to  pudding 87 

Darmstadt,  outbreak  of  food  poisoning  in 100 

de  Nobele,  studies  on  food  poisoning 30 

Dhont,  studies  on  meat  poisoning . . .  .3°>  45 

Dieudonne,  studies  on  enteritidis  and  paratyphoid  bacilli. .       31 

Diseased  meat,  poisoning  due  to,  bacteriology 22 

etiology    20 

historical 16 

v.  Drigalski,  studies  on  meat  poisoning 30 

Durham,  studies  on  meat  poisoning 30,  45 

Diisseldorf,  outbreak  of  meat  poisoning  in 30 

Eber,  test  for  putrefaction 60 

Eberth,   studies   on  meat  poisoning 19 

Eggs,  bacterial  infection  of 86 

Enteritidis  bacillus,  poisoning  by,  clinical  types 41 

diagnosis    44 

prophylaxis    4° 

relation  to  paratyphoid  fever 42 

treatment    47 

Enteritis,    infectious    J5 

v.  Ermengem,  studies  on  meat  poisoning 25,  28,  30,  70 

Exanthem,  in  food  poisoning 18,  78,  87 

Fish,  canned,  as  a  cause  of  poisoning 99 

poisoning,  bacteria  associated  with 73,  74 

symptoms    73,  74 

treatment    of _    79 

roe,  in  food  poisoning 72 


124  INDEX 

PAGE 

Fischer,    studies   on   food   poisoning 27,30,  48,  100 

Fliigge,   studies   on  meat  poisoning 30 

Foot  and  mouth  disease,  relation  to  food  poisoning 20 

Forced  slaughtering,  relation  to  meat  poisoning 21 

see    also    "braxy" 21 

Fornet,  studies   on  pudding  poisoning 88 

Fromme,  studies  on  meat  poisoning 30 

Fruit  acids  and  canned  goods 109 

Fuga,  Japanese  poisonous  fish 72 

Gaffky,  studies  on  food  poisoning 15,  24,  82,  101 

Galeotti,  studies  on  snail  poisoning 77 

Gartner,   studies   on  epidemic  meat  poisoning 23,  25 

Gartner's  bacillus  enteritidis    (see  under  Bacillus) 23 

Gaustad,  outbreak  of  meat  poisoning  in 26 

Gerbstadt,  outbreak  of  meat  poisoning  in 50 

Ghent,  outbreak  of  meat  poisoning  in 28 

Giessen,  outbreak  of  meat  poisoning  in 30 

Gliicksmann,  studies  on  meat  poisoning 51 

Greifswald,  outbreak  of  meat  poisoning  in 30 

Giinther,  studies  on  meat  poisoning 30 

Ffalenke,  lead  in  food  poisoning no 

Hannover,  outbreak  of  meat  poisoning  in 52 

Hatton,  outbreak  of  meat  poisoning  in 30,  45 

Haupt,  studies  on  meat  poisoning 50 

Haustedt,  outbreak  of  poisoning  in 28 

Hay   bacillus,   in   meat   poisoning 54,  69 

Heat,  effect  on  cheese  poison 81 

effect  on  fish  poison 72 

effect  on   mussel   poison 76 

effect  on  poison  of  B.  Aertryck 74 

effect  on  poison  of  B.  botulinus 67 

effect  on  poison  of  B.  enteritidis 23,  24,  25,  26 

effect  on  poison  of  B.  proteus 51,  54 

Heim,  studies  on  bacteria  in  cheese 82 

Heller,  studies  on  meat  poisoning 30 

Hermann,  studies  on  meat  poisoning 30 

Hetsch,  studies  on  paratyphoid  infections 43 

Hoist,   studies   on   food  poisoning 26,81 

Horb,  outbreak  of  meat  poisoning  in 30 

Hiibener,  paratyphoid  and  related  bacilli  in  healthy  animals.       33 

Ice    cream   poisoning 84 

Incubation  period  in  meat  poisoning  and  in  paratyphoid  fever,  43 

in    botulism    68 

Infection,    bacterial    13 

Infectious  enteritis    IS 

Intoxication,    bacterial     13 

Isola,  outbreak  of  snail  poisoning 77 


INDEX  125 

PAGE 

Johne,  studies  on  meat  poisoning 25,  28 

Kaensche,   studies    on   meat   poisoning 30 

Kalamazoo,  outbreak  of  meat  poisoning  in 56 

Kayser,  incubation  period  of  meat  poisoning 43 

Kempner,  studies  on  botulism  antitoxin 68 

Kerner,  studies  on  sausage  poison 62 

Kiel,  outbreak  of  meat  poisoning  in 30 

Kloten,  outbreak  of  meat  poisoning  in ,  18 

Kobert,  on  fish  poisoning ..,  72 

Kutscher,  on  meat  poisoning < 1 .  30 

Lange,  bacterial  infection  of  eggs 87 

Lead,  as  a  cause  of  food  poisoning 108,  no 

in    cans    and    solder 108 

in  glaze  on  earthenware no 

Lehmann,  metallic  poisons  in  food  poisoning 108 

Leipzig,  outbreak  of  food  poisoning 103 

Levy,  studies  on  food  poisoning 50,  88 

Liefmann,  serum  diagnosis  of  meat  poisoning 46 

Lubenau,   on  meat  poisoning 54 

Lustig,   on  mussel  poisoning yy 

Lyons,  outbreak  of  potato  poisoning  in 92 

Malachite   green   agar 37 

Manchester   beer   epidemic 108 

Mansfield,  outbreak  of  meat  poisoning  in 51 

Meat  poisoning,  enteritidis  and  paratyphoid,  diagnosis 44 

prophylaxis     46 

serum    diagnosis    45 

treatment    47 

from  bacillus  botulinus   (see  Botulism) 62 

from  decayed  meat,  diagnosis 58 

frequency     55 

historical    48 

prophylaxis     60 

symptoms     49 

treatment    61 

Meirelbeck,  outbreak  of  meat  poisoning  in 30 

Metallic    poisons,    historical 108 

Meyer,  solanin  content  of  potatoes 93 

Milk,  in  spread  of  paratyphoid  infections 34,  85 

Molluscs,  poisoning  through  eating  of 72 

Moorseele,  outbreak  of  meat  poisoning  in 25 

Morgan,  bacteriology  of  intestinal  tract  in  animals 33 

Mortality,   in   enteritidis   poisoning 41 

in  putrefactive  meat  poisoning 49 

in  potato  poisoning 92 

in    sausage    poisoning 63,  64 

Mouse   typhoid,    bacillus    of 33 


126  INDEX 

PAGE 

Muhlens,  occurrence  of  B.  enteritidis  in  meat 34 

Murex  bradatus   (marine  snail) 77 

Mussel    poisoning    76 

Mytilotoxin,   action   of 76 

Mytilus   edulis    (mussels) 76 


Neelson,  studies  on  meat  poisoning 25 

Neisser,  studies  on  fish  poisoning 74 

Neunkirchen,  outbreak  of  meat  poisoning  in 30 

de  Nobele,  studies  on  meat  poisoning 30 


Oatmeal,  poisoning  through 54 

Ohlmacher,  food  poisoning  through  oatmeal 54 

Ostertag,  history  of  epidemic  meat  poisoning 19 

Owen,  studies  on  food  poison 56 

Oysters,    colon    bacilli    in 78 

capsule  bacilli  in 78 

cholera  transmitted  by 78 

relation  to   food  poisoning 78 

typhoid   transmitted   by 78 

sewage  pollution  of 78,  79 


Paak,  studies  on  meat  poisoning 24 

Partick,  outbreak  of  meat  poisoning  in 24 

Paratyphoid  bacillus    (see   Bacillus  paratyphi) 31,  34,  73 

fever,   relation   to   enteritidis   infections 42 

Pathogenicity  of  typhoid,  paratyphoid  and  enteritidis  bacilli.  37 

of  bacillus   botulinus 67 

of  bacillus   proteus 52 

Pennington,  cold  storage  and  bacterial  multiplication 57 

Peppier,  studies  on  cheese  poisoning 82 

Perkins,  studies  on  cheese  poisoning 80 

Peyer's  patches,  in  meat  poisoning 19,  42 

Pfliiger,  studies  on  cheese  poisoning 82 

Pfluhl,  on  examination  of  canned  goods 105 

on   potato    poisoning 94 

on    proteus    poisoning 52 

Phlebitis  in  calves,  relation  to  meat  poisoning 21 

Pies,  growth   of  typhoid   bacillus 32 

Pike,  as  cause  of  food  poisoning 72,  73,  74 

Plauen,  outbreak  of  meat  poisoning  in 50 

Poels,    studies    on   meat   poisoning 26 

Poisoning  through  decayed  meat • 48 

through  diseased   meat 15 

through    molluscs    72 

Poisonous    fish    72 

Polyarthritis  in  calves,  relation  to  meat  poisoning... 21 

Posen,  outbreak  of  meat  poisoning  in 30 

Pouchet,  studies  on  meat  poisoning 30 


INDEX  127 

PAGE 

Potato  poisoning,  bacteria  associated  with >  95 

historical    91 

prophylaxis    97 

relation  to  solanin   content 92 

treatment    98 

Proteus  bacillus   (see  under  Bacillus  proteus) 48,  51,  95 

Psittacosis,  bacillus  33 

Pudding,  poisoning  through,  bacteriology 85,  86 

prophylaxis 89 

treatment    90 

Putrefaction  of  meat 48 

test  for   59 

Pyaemia  in  calves,  relation  to  meat  poisoning 21 

Rancid  odor,  in  canned  vegetables 102 

Rimpau,  paratyphoid  bacilli  in  healthy  humans 34 

Rodella,  studies  on  bacteria  in  oysters 78 

Roe  of  fish  in  food  poisoning 72 

Roemer,   studies   on  botulism 69 

Roily,    on   food   poisoning 103 

on   paratyphoid   infections 44 

Roseola,  typhoidal,  in  meat  poisoning 18,  88 

Rotterdam,  outbreak  of  meat  poisoning  in 26 

Rumfleth,  outbreak  of  meat  poisoning  in 27 

Salt,  effect  on  growth  of  B.  botulinus 70 

Sausage  poison   (see  Botulism) -    62 

Sausages,  relation  to  meat  poisoning 22 

Scheef,  studies  on  meat  poisoning 30 

Schmiedeberg,  on  potato  poisoning 91 

Schmidtmann,  on  mussel  poisoning 76 

Schneidemuhl,  on  meat  poisoning 20,  50,  75 

Schottelius,    on    canned    goods 106 

Schottmiiller,  on  paratyphoid  infections 43 

Schumburg,  on  meat  poisoning 52 

Secondary  infections  in  epidemic  meat  poisoning. . .  19,  24,  29,  44 

Senkpiehl,  on  sausage  poisoning 64 

Septic  infection  of  cows,  relation  to  meat  poisoning 20 

Sepsis  intestinalis    15 

Serum   diagnosis   in  epidemic  meat  poisoning 24,45 

in   fish    poisoning 73,  74 

in  food  poisoning 86 

treatment  for  botulism 68,  71 

Sheppard,   on   botulism 64 

Silberschmidt,  on  food  poisoning 30,  73 

Sirault,  outbreak  of  meat  poisoning  in 30 

Snail    poisoning    yy 

Solanin    content    of   potatoes 93 

poisoning    92 

Staphylococcus  in   meat  poisoning 56 

Sturgeon,  as  a  cause  of  food  poisoning 72 


128  INDEX 

PAGE 

Subtilis  bacillus  in  meat  poisoning 54 

Swine  erysipelas,  bacillus  of,  in  cheese  poisoning 82 

Temperature,  effect  of,  on  production  of  botulinus  toxin. .     102 

on    proteus    toxin 95 

Tin,    in   food   poisoning 108 

Toxin   of  bacillus   Aertryck 74 

botulinus      67,  68 

coli     48 

enteritidis     23 

proteus 49,  95 

cheese  poisoning   81 

Trautmann,    studies   on  meat  poisoning 30,   41 

Tubercle  bacilli   in  cheese 82 

Typhoid  bacillus,  biological  characteristics  of 35 

in   cheese,    viability    of 82 

resemblance    to    enteritidis    bacillus 27 

Typhoid    fever,   and   oysters 78 

resemblance  of  meat  poisoning  to 19 

Tyrotoxicon,  in  cheese  poisoning 80 

Uhlenhuth,  on  meat  poisoning 30 

on  paratyphoid  bacilli  in  intestines  of  hogs 33 

Ulrich,  on  fish  poisoning 73 

Urticaria,  in  food  poisoning 18,  78 

Vagedes,  detection  of  bad  oysters 79 

on  paratyphoid  poisoning  through  pudding 85 

van  Ermengem,  on  meat  poisoning 25,  26,  28,  40,  70 

Vanilla,  in  ice  cream  and  pudding  poisonings 84 

Vegetables,  canned,  in  food  poisoning 100 

Virchow,  on  mussel  poisoning j6 

Vivaldi,  bacteria  in   oysters 78 

von  Drigalski,  on  meat  poisoning 30 


Wassermann,  antitoxin  for  botulism 71 

Weil,  on  solanin  content  of  potatoes 93 

Weil's    disease 20 

Wesenberg,  on  meat  poisoning 51 

Widal  test  (see  Serum  diagnosis) 45 

Wildbad,  sausage   poisoning  in 63 

Wilhelmshaven,  outbreak  of  mussel  poisoning  in j6 

Wintgen,  on  potato  poisoning 93 

Wiirttemberg,  sausage  poisoning  in 63 

Wyss,   on  fish  poisoning 73 

Zardo,  on  mussel  poisoning 77 

on  snail  poisoning yy 

Zupnik,   typhoidal   meat   poisoning 44 

Zurich,    outbreak  of  fish  poisoning  in J2 


RA1260 
DieudonnS 


D56 


